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Physiology > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

general function of respiratory system

A

to obtain O2 for use by the body’s cells, and to eliminate the CO2 the body’s cells produce

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2
Q

what is another name for internal respiration

A

cellular respuration

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3
Q

describe internal respiration

A
  • oxidative phosphorylation
  • refers to metabolic processes and carried out within the mitochondria, which use O2 and produce CO2 while deriving energy from nutrient molecules
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4
Q

four steps of external respiration

A
  1. has exchange between the atmosphere and alveoli in the lung
  2. exchange of O2 and CO2 between air in the alveoli and the blood in the pulmonary capillaries
  3. Transport of O2 and CO2 by the blood between the lungs and the tissues
  4. Exchange of O2 and CO2 between the blood in the systematic capillaries and the tissue cells
    * respiration occurs now
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5
Q

seven secondary functions of the respiratory system

A
  • Short term pH regulation
  • Enables vocalisation
  • Aids in defense againt pathogens in the airways
  • Removes, modifies, activates (i.e. angiotensin II), or inactivates (i.e. prostaglandins) various materials passing through the pulmonary circulation
  • Eliminates heat and water
  • Assists venous return
  • Nose is the organ of smell
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6
Q

three componenents of upper airways

A
  • Nasal cavity
  • Oral cavity
  • Pharynx (common passageway for respiratory and digestive systems)
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7
Q

three componenents of respiratory airways

A
  • Larynx
  • Conducting zone
  • Respiratory zone
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8
Q

important point of conduction zone

A

it’s an anatomical dead space

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9
Q

why is the conducting zone an anatomical dead space

A

no gases are exchanged even though air is moving through it

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10
Q

what does the respiratory zone consist of

A

bronchi, bronchioles and alveoli

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11
Q

six structures of the conducting zone

A
  • trachea
  • primary bronchi
  • secondary bronchi
  • tertiary bronchi
  • bronchioles
  • terminal bronchioles
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12
Q

dimensions of the trachea

A

2.5 cm diameter, 10 cm long

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13
Q

what is the trachea made up of

A

C-shaped bands of cartilage for structural rigidity

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14
Q

how many secondary bronchi on the right side

A

3

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15
Q

how many secondary bronchi on the left side

A

2

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16
Q

bronchiole diameter

A

less than 1mm

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17
Q

functions of the conducting zone

A
  • Air passageway (150ml volume - dead space)
  • Increase air temperature to body temperature
  • Humidify air
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18
Q

two types of cells in the conducting zone

A

goblet and cilliated

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19
Q

important point about bronchiole composition

A

they have no cartilage, thus there is a risk of collapse
to prevent this they have walls of elastic fibres and smooth muscle

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20
Q

goblet cell function

A

secrete mucus and traps foreign particles

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21
Q

cilliated cell function

A

propel the mucus up the glottis to be swallowed or expelled

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22
Q

clinical consideration regarding cilliated cells

A

Smoking stops cilliated cells from working as effectively - thus smokers cough a lot

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23
Q

four main structures of respiratory zone

A
  • Respiratory bronchioles
  • Alveolar ducts
  • Alveolar sacs
  • Alveoli
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24
Q

function of respiratory zone

A

Exchange of gases between air and blood by diffusion

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25
Q

what are alveoli

A

site of gas exchange

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26
Q

what is the respiratory membrane made up of

A
  • Alveoli: Type 1 cells and basement membrane
  • Capillaries: Endothelial cells and basement membrane
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27
Q

how many alveoli per lung

A

200-500 million

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28
Q

comment on blood supply of alveoli

A

They have a rich blood supply as capillaries form a sheet over each alveolus

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29
Q

what is collateral ventilation

A

alveoli have pores (pore of Kohn) which permit airflow between adjacent alveoli in case one stops working

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30
Q

name the three alveoli cell types

A
  • type I alveolar cells
  • type II alveolar cells
  • alveolar macrophages
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31
Q

function of type I alveolar cells

A

Make up wall of alveoli, single layer epithelial cells

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32
Q

function of type II alveolar cells

A
  • Secrete surfactant
  • Reduces surface tension in alveolar walls
  • Helps prevent alveolar collapse
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33
Q

purpose of alveolar macrophages

A

Remove foreign particles

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34
Q

how thick is the respiratory membrane

A

0.2 microns

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35
Q

name the three main pressure considerations

A
  • atmospheric pressure
  • intra-alveolar pressure
  • intrapleural pressure
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36
Q

another name for atmospheric pressure

A

barometric

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37
Q

another name for intra-alveolar pressure

A

intrapulmonary pressure

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38
Q

another name for intrapleural pressure

A

intrathoracic

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39
Q

what is atmospheric pressure at sea level (in mmHg)

A

760 mmHg

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40
Q

what is the relationship between atmospheric pressure and altitude

A

as altitude increases atmospheric pressure decreases

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41
Q

what is intra-alveolar pressure

A

pressure of air within alveoli in the lungs

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42
Q

is intra-alveolar pressure an open or closed system

A

open

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43
Q

what is intra-alveolar pressure during inspiraion

A

negative - less than atmospheric pressure

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44
Q

what is intra-alveolar pressure during expiration

A

positive - more than atmospheric pressure

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45
Q

what drives ventilation

A

the difference between intra-alveolar pressure (Palv) and atmospheric pressure Patm

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46
Q

what is intra-pleural pressure

A

pressure inside teh pleural sac

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47
Q

is intra-pleural pressure an open or closed system

A

closed

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48
Q

what is intrapleural pressure at rest (in mmHg)

A

756 (-4) mmHg

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49
Q

why is intrapleural pressure negative

A
  • due to the elacisity in the lungs and chest wall
    • Lungs recoil inward
    • Chest walls recoil outwards
    • Opposing forces pull on the intrapleural space
    • The surface tension of the intrapleural fluids holds the wall and lungs together - this si because H2O molecules are polar and attract eachother
    • Sub-atmospheric pressure is due to a vacuum in the pleural cavity
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50
Q

what does at rest mean

A

between breaths - no movement of air

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51
Q

how to calculate teh transmural pressure gradient across teh lung wall

A

the intra-alveolar pressure take away the intrapleural pressure

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52
Q

how to calculate the transmural pressure gradient across the thoracic wall

A

the atmospheric pressure take away the intrapleural pressure

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53
Q

what is a pneumothorax

A

a punctured lung

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54
Q

how does a pneumothorax occur

A
  • Occurs when pleural cavity is punctured
  • It looses its negative pressure
  • The lung then collapses
  • The thorax expands
  • Only happens to one lung because the pleural sacs are seperate
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55
Q

two types of pneumothorax

A

traumatic and spontaneous

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56
Q

explain traumatic pneumothorax

A
  • Puncture wound in chest wall
  • Can come about due to a stab wound
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57
Q

explain spontaneous pneumothorax

A
  • Caused by a hole in the lung
  • Can be caused by emphesma
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58
Q

boyle’s law

A

pressure is inversely related to volume in an airtight container (closed system) - therefore, if the volume doubles, the pressure halves

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59
Q

mechanics of breathing formula

A
  • R = resistance to airflow - this resistance is related to the radius of airways and mucus
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60
Q

two factors determining intra-alveolar pressure

A
  • Quantity of air in alveoli
  • Volume of alveoli
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61
Q

waht happens to intra-alveolar pressure during inspiration

A
  • Lungs expand - therefore volume of alveolar pressure increases (this requires muscles)
  • Palv decreases
  • Pressure gradient forces air into the lungs
  • Quantity of air in the alveoli rises
  • Palv increases
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62
Q

what happens to intra-alveolar pressure during expiration

A
  • Lungs recoil - therefore alveolar volume decreases (passive - no muscles required)
  • Palv increases
  • Pressure gradient forces air out of lungs
  • Quantity of air in the alveoli decreases
  • Palv decreases
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63
Q

what is happening to muscles before inspiration

A
  • External intercostal muscles are relaxed
  • Diaphragm is relaxed
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64
Q

what are muscles doing during inspiration

A
  • External intercostal muscles contract
  • Contraction of external intercostal muscles causes rib elevation, increasing side-to-side dimension of thoracic cavity
  • Rib cage becomes elevated
  • Elevation of ribs causes sternum to move up and out, increasing front-to-back dimension of thoracic cavity
  • Diaphragm contracts
  • Lowering of diaphragm upon contraction increases vertical dimension of thoracic cavity
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65
Q

what are muscles doing during passive expiration

A
  • Relaxation of external intercostal muscles
  • Relaxation of diaphragm
  • Return of diaphragm, ribs and sternum to resting position on relaxation of inspiratory muscles restores thoracic cavity to pre-inspiratory size
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66
Q

what are muscles doing during active expiration

A
  • Contraction of internal intercostal muscles
  • This flattens ribs and sternum, further reducing side-to-side and front-to-back dimensions of thoracic cavity
  • Contraction of abdominal muscles
  • This causes diaphragm to be pushed upward, further reducing vertical dimension of thoracic cavity
  • All of this creates higher air pressure, facilitating increased air flow
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67
Q

what are the principle muscles of inspiration

A
  • External intercostals - elevate ribs
  • Interchondral part of internal intercostals - elevate ribs
  • Diaphragm - domes descend, increasing longitudinal dimension of chest and elevating lower ribs
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68
Q

what are teh accessory muscles of inspiration

A
  • Sternocleidomastoid - elevates sternum
  • Scalenus (anterior, middle and posterior) - elevate and fix upper ribs
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69
Q

why are there no muscles involved in quiet expiration

A

because it results from passive recoil of lungs

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70
Q

what are the muscles involved in active expiration

A
  • Internal intercostals except interchondral part
  • Abdominal muscles - depress lower ribs, compress abdominal contents
  • Rectus abdominus
  • External Oblique
  • Internal oblique
  • Transversus abdominus
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71
Q

two factors affecting pulmonary ventilation

A
  • lung compliance
  • airway resitance
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72
Q

what is lung compliance

A
  • Ease with which lungs can be stretched
  • The less compliant the lungs are, the more work is required to achieve a given degree of inflation
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73
Q

what is lung compliance affected by

A

elasticity and surface tension of lungs

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74
Q

what is airway resistance affected by

A

passive forces, contractile activity of smooth muscle and mucus secretion

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75
Q

how much of total energy expenditure does quiet breathing require

A

3%

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76
Q

four times the work of breathing is increased

A
  • When pulmonary compliance is decreased
  • When airway resistance is increased
  • When elastic recoil is decreased
  • When there is a need for increased ventilation
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77
Q

what is tidal volume

A

amount of air moved in and ou in quiet breath

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78
Q

tidal volume total

healthy adult male

A

500ml

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79
Q

what is inspiratory reserve volume

A

amount of air which can be breathed in at once

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80
Q

inspiratory reserve volume total

healthy adult male

A

3000ml

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81
Q

what is inspiratory capacity

A

anount of air that fits in lings

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82
Q

what is inspiratory capacity total

healthy adult male

A

3500ml

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83
Q

what is expiratory reserve volume

A

amount of air that can be breathed out aditionally

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84
Q

wah is expiratory reserve volume total

healthy adult male

A

1000ml

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85
Q

what is residual volume

A

air left in lungs (cannot be measured by a spirometer)

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86
Q

what is residual volume total

healthy adult male

A

1200ml

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87
Q

what is functional residual capacity

A

volume after quiet expiration

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88
Q

what is funcitional residual capacity total

healthy adult male

A

2200ml

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89
Q

what is vital capacity

A

how much air can be breathed out from maximal expiration

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90
Q

what is vital capacity total

A

4500ml

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91
Q

what is total lung capacity

A

total air that can be breathed in or out

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92
Q

what is total lung capacity total

healthy adult male

A

5700ml

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93
Q

pulmonary minute ventilation

A

total volume of air entering and leaving the respiratory system wach minute

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94
Q

minute ventialtion calculations

A
  • Minute ventilation = tidal volume x RR
  • Normal rate of respiration = 12 breaths
  • Normal tidal volume = 500ml
  • Normal minute ventilation = 500ml x 12 breaths/min = 6000ml
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95
Q

alveolar minute ventilation

A

Volume of air exchanged between the atmosphere and the alveoli per minute

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96
Q

alveolar minute ventilation calculations

A

Alveolar ventilation = (tidal volume - dead space) x RR = (500-150)ml x 12 breaths/min = 4200ml

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97
Q

which is more important: alveolar or pulmonary minute ventilation

A

alveolar

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98
Q

Which is smaller: alveolar or pulmonary minute ventilation and why

A

Less than pulmonary ventilation due to anatomical dead space

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99
Q

what does CO2 do to increase airflow when there is large blood flow and small airflow

A

increase in Co2 in area → relaxation of local airway smooth muscle → dilation of local airways → decrease in airway resistance → increase in airflow

100
Q

what does O2 do to decrease blood flow when there is large blood flow and small airflow

A

decrease in O2 in area → increase in contraction of local pulmonary-arteriolar smooth muscle → constriction of local blood vessels → increase in vascular resistance → decrease in blood flow

101
Q

what does CO2 do to reduce airflow when there is large airflow and small blood flow

A

decrease of CO2 in area → increase in contraction of local airway smooth muscle → constriction of local airways → increase in airway resistance → decrease in airflow

102
Q

what does O2 do to increase bloodflow when there is large airflow but low blood flow

A

increase in O2 in area → relaxation of local pulmonary-arteriolar smooth muscle → dilation of local blood vessels → decrease in vascular resistance → increase in blood flow

103
Q

what is ventilation

A

airflow

104
Q

what is perfusion

A

blood supple

105
Q

what is the ventilation in L/min at the top of the lung

A

0.24

106
Q

what is the perfusion in L/min at the top of the lung

A

0.07

107
Q

what is the ventilation - perfusion ratio at the top of the lung

A

3.40

108
Q

what is ventilation in L/min at the bottom of the lung

A

0.82

109
Q

what is perfusion in L/min at the bottom of the lung

A

1.29

110
Q

what is the ventilation-perfusion ratio at the bottom of the lung

A

0.63

111
Q

why is perfusion higher than ventilation at the bottom of the lung

A

because gravity affects perfusion more than ventilation (blood vs air)

112
Q

two main classifications of respiratory diseases

A

obstructive and restrictuve

113
Q

what occurs in obstructive diseases

A
  • Airway narrowing
  • Increased airway resistance
  • Reduced flow during expiration
114
Q

three examples of obstructive respiratory diseases

A

emphysema, chronic bronchitis, asthma

115
Q

explain restrictive respiratory dieases

A
  • Reduced compliance (ease with which we expand the lungs)
  • Scar tissue formation
  • Fibrosis
116
Q

an example of a restrictive respiratory disease

A

pulmonary fibrosis

117
Q

four other respiratory conditions

not classed as restrictive or obstructive

A
  • Diseases impairing diffusion of O2 and CO2
  • Neuromuscular disorders
  • Inadequate perfusion
  • Ventilation-perfusion imbalances
118
Q

explain asthma

A
  • Airway hyper-reactivity
  • Reversible airway narrowing
  • Muscous thickening
  • Smooth muscle constriction by spasms in small airways
  • Most common childhood respiratory disease
  • When severe, narrowing could be lethal
119
Q

causes of asthma

A
  • Allergens, pollens, animal fur, dust
  • Smoking, smog, airborne pollutants
  • Changes in air temperature, humidity, pressure
  • Exercise
  • Emotional stress, anxiety
120
Q

treatment of asthma

A

bronchodilators, anti-inflammatory. O2

121
Q

is asthma obstructive or restrictive

A

obstructive

122
Q

explain chronic bronchitis

A

-Inflammation of airway walls
- Excessive mucous production
- Airway narrowing and coughing (cough does not remove mucous)
- Reversible

123
Q

Causes of chronic bronchitis

A
  • Bacterial and viral infections
  • Smoking
  • Airborne pollutants
  • Chronic irritation (seen in miners)
124
Q

is chronic bronchitis obstructive or restrictive

A

obstructive

125
Q

explain emphysema

A
  • Irreversible
  • Destruction of alveolar walls (collapsing of small airways)
  • Enlargement of air spaces
    • Primarily distal to terminal bronchioles
  • Increased lung compliance via:
    • Destruction of elastic fibres
    • Excessive release of the enzyme trypsin - macrophages secrete α anti-trypsin to inhibit trypsin, but with chronic irritation trypsin can break alveolar walls
126
Q

causes of emphysema

A
  • Smoking induced inflammation
  • Cilia destruction, tar accumulation
  • Airborne contaminants
  • Genetic - lack of α anti-trypsin production
127
Q

is emphysema obstructive or restrictive

A

obstructive

128
Q

explain pulmonary fibrosis

A
  • Diffuse Interstitial Lung Disease (DILL) - larger type of diseases
  • Results from over 130 disorders
  • Reduced elasticity
  • Reduced compliance of lung and chest wall
  • Increased work of breathing
  • Slim patients - breathing takes up a lot of their energy
129
Q

causes of pulmonary fibrosis

A
  • No known cause in 2/3 of cases
  • Breathing in asbestos fibres
  • Inflammation
  • Scar tissue formation
130
Q

is pulmonary fibrosis restrictive or obstructive

A

restrictive

131
Q

total lung capacity in obstructive dieases

A

normal or increased

132
Q

total lung capacity in restrictive dieases

A

decreased

133
Q

residual volume in obstructive diseases

A

very increased - lungs cannot empty properly

134
Q

residual volume in restrictive dieases

A

normal or decreased

135
Q

vital capacity in obstructive diseases

A

decreased

136
Q

vital capacity in restrictive diseases

A

decreased

137
Q

functional residual capacity in obstructive diseases

A

inreased

138
Q

functional residual capacity in restrictive diseases

A

normal or decreased

139
Q

inspiratory capactiy in obstructive diseases

A

decreased

140
Q

inspiratory capacity in restrictive diseases

A

very decreased

141
Q

obstructive or restrictive and why

A

obstructive as FRC is larger than normal as lungs cannot be emptied as fast as they should be

142
Q

obstructive or restrictive

A

obstructive

143
Q

obstructive or restrictive and why

A

IRV is much lower than normal - inspiratory effort is compromised which reduced total lung capacity

144
Q

obstructive or restrictive

A

restrictive

145
Q

what is total pressure of gases

A

the sum of all partial pressures

146
Q

what does the partial pressure of a gas depend on

A
  • Fractional concentration of the gas
  • Total pressure of the gas mixture
147
Q

gas composition of air at 0% humidity

A
148
Q

composition of gas in air at 100% humidity

A
149
Q

rate of diffusion formula

A

Vgas = rate of diffusion
A = surface area (normally between 50 and 100 mm2 in lung)
T = thickness (normally 0.2-0.5µm)
ΔP = pressure difference
D = diffusion constant

150
Q

diffusion constant formula

A

S = gas solubility
MW = molecular weight

151
Q

gas solubility of CO2

A

24

152
Q

gas solubility of O2

A

1

153
Q

molecular weight of CO2

A

44

154
Q

molecular weight of O2

A

32

155
Q

how long is capillary transit time (blood in capilary) at rest

A

0.75 seconds

156
Q

what is equilibration time reduced to during intense exercise

A

0.25 seconds

157
Q

two things that affect the diffusion process in the lung

A
  • exercise
  • thickening of blood-gas barrier
158
Q

what pathology are highly-trained athletes at risk of

A

Exercise Induced Arterial Hypoxemia (EAIH)

159
Q

What is Pulmonary Oedema

A

Fluid accumulation in alveoli and/or interstitial space

160
Q

what does pulmonary oedema do

A
  • Impairs diffusion (greater distance from alveoli to blood)
  • Leakage in unprotected capillaries
  • Increases work of breathing (decreased lung compliance)
  • Arterial blood: lower PO2 and higher PCO2
161
Q

causes of pulmonary oedema

A
  • Increased capillary pressure via left heart failure (inability to supply sufficient blood flow)
  • Reduced atmospheric pressure at altitude
162
Q

treatment of pulmonary oedema

A

administering oxygen and diuretics

163
Q

how many mls of oxygen in every litre of arterial blood

A

200ml

164
Q

what percentage of O2 in blood is dissolved in plasma

A

1.5%

165
Q

what percentage of oxygen in arterial blood is bound to haemoglobin

A

98.5%

166
Q

structure of haemoglobin

A

Four sub-units - each with one haem group and one globin

167
Q

oxyhaemoglobin

A

Haemoglobin bound to oxygen

168
Q

deoxyhaemoglobin

A

Unbound haemoglobin

169
Q

function of haemoglobin

A

to increase oxygen-carrying capability of blood

170
Q

where is haemoglobin found

A

red blood cells

171
Q

what is the Hemoglobin-Oxygen Dissociation Curve

A

a graph that displays how easily oxygen is bound and unbound to haemoglobin

172
Q

waht does a shift of the haemoglobin-oxygen dissociative curve to the right indicate

A
  • decreased affinity meaning a higher PO2 is required to achieve a level of oxygen saturation
    • Oxygen is unloaded more easily from haemoglobin, making it more available to tissues
173
Q

what does a shift of the haemoglobin-oxygen dissociative curve to the left indicate

A
  • increased affinity meaning a lower PO2 is required to achieve a level of oxygen saturation
    • Oxygen is loaded more easily onto haemoglobin
174
Q

what percentage of carbon dioxide is dissolved

A

10%

175
Q

what percentage of carbond dioxide is bound to haemoglobin

A

30%

176
Q

what percentage of carbon dioxide is transported in the form of bicarbonate ios

A

60%

177
Q

carbon dioxide transport formula

A
178
Q

hypoxia

A

Insufficient cellular O2

179
Q

hyperoxia

A

Too much arterial O2 - O2 toxicity

180
Q

hypocapnia

A

Excess PaCO2

181
Q

hypocapnia

A

Below normal PaCO2

182
Q

Model of Respiratory Control During Quiet Breathing

A

sensory input/pons/cortex → central pattern generator (medulla) → inspiratory neurons of DRG and VRG (medulla → breathing rhythm

183
Q

what do chemoreceptors detect

A

PO2 and PCO2 changes

184
Q

what do pulmonary stretch receptors detect

A

(Hering-breuer reflex): Inflation and deflation

185
Q

what do irritant receptors detect

A

Dust and pollutants (trigger coughing/sneezing)

186
Q

two types of chemoreceptor

A

central and peripheral

187
Q

peripheral chemoreceptor location

A
  • Carotid bodies - near baroreceptors in carotid sinus
  • Aortic bodies - aortic arch
188
Q

peripheral chemoreceptor function

A
  • Respond to decreasing PaO2 (less than 60mmHg) - this is crucial when at an altitude
  • Respond to increasing PaCO2 and increasing H+ - this provides 20% of respiratory drive
  • Aortic bodies (although rarely) respond to decreasing total arterial O2 content - crucial for anaemia and carbon monoxide poisoning
189
Q

central chemoreceptor loaction

A

medulla

190
Q

central chemoreceptor function

A
  • Directly respond to changes in H+ concentration in the CSF
    • Specifically those ions converted from CO2 - not those circulating as they cannot cross the blood-brain barrier
  • Therefore they indirectly respond to changes in the PaCO2
  • Provide 80% of the respiratory drive
191
Q

effects of arterial O2 on ventilation

A
  • Declining arterial PO2 has little effect on minute ventilation until PO2 drops to less than 60 mmHg
  • Response is due to the activation of peripheral chemoreceptors
192
Q

Effects of Arterial CO2 on Ventilation

A
  • Increasing arterial PCO2 has large effects on minute ventilation
  • At a PCO2 greater than 90mmHg, coma and death can occur
  • Effects are mediated through both central and peripheral chemoreceptors but Co2 must be converted to H+ first
193
Q

Effects of Hypoventilation on Minute Ventilation

A

increasing PCO2, increasing H+ and decreasing PO2 in arterial blood → chemoreceptors detect and respond → respiratory control centre increases ventilation → negative feedback to step 1

194
Q

Effects of Hyper-ventilation on Minute Ventilation

A

decreasing PCO2, decreasing H+ increasing PO2 in arterial blood → chemoreceptors detect and respond → respiratory control centre decreases ventilation → negative feedback to step 1

195
Q

arterial pH

A

7.4

196
Q

how does C2 maintain pH balance

A
  • pH is directly related to H+ ion concentration
  • CO2 is a source of H+ ions
197
Q

acidosis

A

when arterial blood is excessively acidic - pH greater than 7.0

198
Q

what does acidosis cause

A
  • Depresses CNS activity
  • Progress to coma and respiratory failure
199
Q

alkalosis

A

when blood is excessively alkaline or basic

200
Q

what does alkalosis do

A
  • Increases CNS excitability causing uncontrollable muscle seizures and convulsions
  • Can lead to death as a result of spasmodic contraction of respiratory muscles
200
Q

bronchiole response to increased PcO2

A

Dilation (increased ventilation)

201
Q

pulmonary arteriole response to increased PCO2

A

Weak constriction (decreased perfusion)

202
Q

bronchiole response to decreased PCO2

A

Constriction (decreased ventilation)

203
Q

Pulmonary arteriole response to decreased PCO2

A

Weak dilation (increased perfusion)

204
Q

bronchiole response to increased PO2

A

Weak constriction (decreased ventilation)

205
Q

pulmonary arteriole response to increased PO2

A

Dilation (increased perfusion)

206
Q

Bronchiole response to decreased PO2

A

Weak dilation (increased ventilation)

207
Q

pulmonary arteriole response to decreased PO2

A

Constriction (decreased perfusion)

208
Q

cause of hyperventilation

A

decreased PaO2 acting on carotid body peripheral chemoreceptors - hypoxic ventilatory drive

209
Q

body’s response to hyperventilation

A
  • CO2 clearance increases → blood pH increases → respiratory alkalosis (reduced ventilation)
  • To prevent alkalosis: kidneys excrete bicarbonate ions → more acid remains in blood → alkalosis is reversed → pH is normal within 2-3 days
  • Ventilation then increases again
    • Reason for maintained ventilation is unknown
    • Likely increases sensitivity to PaO2
210
Q

what is Polycythaemia

A
  • Increased red blood cell concentration in blood
  • Increased haemoglobin content in blood
211
Q

body’s repsonse to Polycythaemia

A
  • Decreased PaO2 (hypoxemia) stimulates erythropoietin (EPO) after about 3 hours (the peak is 24-48 hours)
    • This comes from the kidney
    • It acts in bone marrow
    • Stimulate:
      • Reticulocyte maturation and release
      • Erythropoiesis
  • Despite a decrease in PaO2 and thus a decrease in haemoglobin saturation (by the oxygen-haemoglobin dissociation curve) total O2 content may be normal or elevated
212
Q

what causes elevated blood viscosity

A

Polycythaemia

213
Q

what does elevated blood viscosity cause

A
  • Increase in cardiac work (hypertrophy)
  • Uneven blood flow distribution
214
Q

what other adaptations to high altitudes are there

A
  • Improved diffusion capacity via:
    • Expanded surface area due to greater lung volume upon inflation
    • Increased tissue capillarisation (angiogenesis) - occurs over days
  • Endothelial cells release up to 10 times more nitric oxide (NO)
  • Reduced skeletal muscle fibre size - occurs over weeks
    • In conjunction with increased oxidative capacity and mitochondria numbers
215
Q

symptoms of acute mountain sickness

A
  • Headaches
  • Loss of appetite
  • Insomnia
  • Nausea
  • Vomiting
  • Dyspnea
216
Q

when is onset of actute mountain sickness symptoms

A

6-48 hours after ascent

216
Q

when do the most severe sympotoms of acute mountain sickness occur

A

on days 2 and 3

217
Q

why is acute mountain sickness worse at night

A

respiratory drive is reduced

218
Q

what does incidence of acute mountain sickness vary by

A

altitude, rate of ascent and the individual’s susceptibility

219
Q

what percentage of people experience symptoms of acture mountain sickness at elevations of 2,500-3,500 metres

A

15% but higher in women

220
Q

what percentage of people experience symptoms of acute mountain sickness at elevations of greater than 3,500 metres

A

75% of individuals at least mild symptoms

221
Q

what causes high altitude pulmonary oedema

A

pulmonary vasoconstriction (hypoxia)

222
Q

what does high altitude pulmonary oedema lead to

A
  • Fluid accumulation leads to persistent cough, shortness of breath, cyanosis of lips and fingernails and loss of consciousness.
  • Could lead to high altitude cerebral oedema (fluid accumulation in cranial cavity)
223
Q

treatment of high altitude pulmonary oedema

A

descending to lower altitude and supplemental oxygen

224
Q

name four Altitude/Hypoxic Training Strategies to Maximise Sea-Level Performance in Athletes

A
  • Live high – train high (LHTH or HiHi)
  • Live (or sleep) high – train low (LHTL or HiLo)
  • Live low – train high (LLTH or LoHi)
  • Intermittent hypoxia at rest
225
Q

describe live high-train high

A
  • Benefit: increase red blood cell volume (>2000m x 3-4 weeks)
  • Problem: difficult to train at same volume/intensity as at sea level
  • There are few well controlled studies on elite athletes
226
Q

describe live high -train low

A
  • Most effective (altitude: 2100-2800m x 3-4 weeks)
  • Problem: logistics and financial
  • New modalities: Hypoxic tents (sleeping devices) or even hypoxic living apartments (>2000m x 3 weeks x >12h/day)
227
Q

effects of live low-train high

A

weak if any

228
Q

effects of intermittent hypoxia at rest

A

weak if any

229
Q

what happens to gas pressures at depth

A
  • total gas pressure increases
  • partial gas pressures increase as well
230
Q

what problems are caused to gas cavities (lung, middle ear) by increasing pressures at depth

A
  • Compression with descent
  • Over-expansion with ascent
231
Q

nitrogen solubility at sea level

A
  • N2 is poorly soluble
  • Low amounts of dissolved N2 - no adverse effects
232
Q

nitrogen solubility at depth

A
  • Increase in N2 partial pressures → increase in N2 solubility
  • This leads to a high amount of N2 being dissolved in blood, influencing ion regulation and excitable cells
233
Q

nitrogen narcosis cause

A

Increased N2 solubility → reduced neuron excitability → nitrogen narcosis

234
Q

nitrogen narcosis effects at 50m (150 ft)

A

“Cocktail” effect (euphoria and drowsiness)

235
Q

nitrogen narcosis effects at 50-90m (150 - 300 ft)

A
  • Fatigued and weak
  • Loss of coordination
  • Clumsiness
236
Q

nitrogen narcosis effects at 100-120m (350 - 400 ft)

A

Lose consciousness

237
Q

prevention of nitrogen narcosis

A
  • Use N2 free gas
  • Substitute helium for N2 because its solubility is ½ that of N2
  • 100% O2 is not appropriate due to O2 toxicity
238
Q

how does decompression sickenss occur

A
  • Occurs during rapid ascent and decreasing pressure
  • As N2 suddenly becomes less soluble, it comes out of its solution
  • These leads to the formation of bubbles (Champagne cork effect)
  • Its effects depend on the size and location of the bubbles
239
Q

effects of nitrogen narcosis when it cuases a gas embolus in circulation

A
  • tissue ischaemia
    • May be critical in Brain, Coronary or Pulmonary circulations
    • Avascular necrosis common in head of femur
240
Q

effects of decompression sickness when it causes bubble formation in the myelin sheath

A

Compromise nerve conduction (dizziness, paralysis)

241
Q

decompression sickness effects whe it cuases bubble/gas expansion

A
  • Muscle and joints (The Bends): severely painful
  • Ear: vestibular disturbances, deafness
  • Lung: tissue rupture (airway bursting)
242
Q

decompression sickness prevention

A
  • Slow ascent
  • N2 gas replacement
  • Exhale during ascent
243
Q

decompression sickness treatment

A

recompression

Physiology (6 decks)

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