Respiratory Systems Flashcards

1
Q

What is ventilation?

A

The process of shifting air from the outside world into your lungs (which is technically still the outside world but just inside your body because there is no skin between inside the alveoli and the outside world).

It is the supply of O2 to and removal of Co2 from the alveoli.

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2
Q

What are the two types of gas exchange during respiration?

A

1) The exchange of O2 and CO2 across the alveolar membrane = air to blood (e.g., air to inside the body across skin layer)

and then

2) the exchange of O2 and CO2 between the capillaries and the cells

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3
Q

What is respiration?

A

The exchange of O2 and CO2 between the tissues and the environment

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4
Q

What are the 5 steps of respiration?

A

1) Ventilation
2) Gas exchange
3) Gas transport
4) Gas exchange
5) cellular respiration

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5
Q

What is gas transport?

A

Deliver O2 from lungs to tissues and transport CO2 produced by metabolism to the lungs (cardiorespiratory).

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6
Q

What is cellular respiration?

A

The cells use of O2 and production of Co2 (metabolism)

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7
Q

What processes in respiration are bulk flow?

A

Ventilation and gas transport

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8
Q

What are the functions of the respiratory system?

A

Provide Oxygen
Eliminate Carbon Dioxide
Filters, warms and humidifies the air we breath
Communication
Sense of smell
Regulate the pH of the blood in association with the kidneys
Defend against microbes
Temperature regulation

(PEFCSRDT)

please eliminate fat cunts so raewyn doesn’t tumble

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9
Q

What are the muscles used during inspiration?

A

Sternomastoid
Scalene’s Muscles
External intercostals
Diaphragm

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10
Q

What are the muscles used during expiration?

A

Internal intercostals
External oblique abdominal rectus

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11
Q

What does the sternomastoid do?

A

elevate the sternum

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12
Q

What do the scalene’s muscles do?

A

elevate the upper ribs

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13
Q

What direction does the diaphragm move as it contracts?

A

Descends

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14
Q

What do the external intercostals do?

A

Elevate the ribs

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15
Q

What do the internal intercostals do?

A

Depress the ribs

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16
Q

What does the external oblique abdominal rectus do?

A

External oblique abdominal rectus = abdominal muscles

Recruited for very deep and forceful expiration.

They depress the lower ribs and compress the viscera.

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17
Q

What is expiration caused by?

A

Caused by lung elastic recoil pulling the thorax and relaxed diaphragm inwards.

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18
Q

Is there muscle contraction during restful expiration?

A

No it is passive

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19
Q

What is happening during inspiration and expiration of deep breathing?

A

Inspiration is the contraction of the diaphragm and external intercostal muscles

Expiration is lung elastic recoil and internal intercostal muscle contraction

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20
Q

What additional muscles are recruited for very deep forceful breaths inspiration and expiration?

A

Sternocleidomastoid and pectorals minor muscles for inspiration.

Abdominal muscles for expiration.

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21
Q

What is the pleura?

A

A thin layer of tissue that covers the lungs and lines the interior wall of the chest cavity.

it forms an envelope between the lungs and the chest wall.

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22
Q

What is the parietal pleura and visceral pleura?

A

Parietal pleural = outer layer that lines the chest wall and diaphragm

Visceral pleura = inner layer that is directly on the lungs lining the outside.

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23
Q

What is the pleural cavity filled with?

A

Pleural fluid

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24
Q

Are the lungs and chest wall attached?

A

No (the lungs are always wanting to pull away from the chest wall).

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25
Q

What is P atm?

A

Atmospheric pressure (can also be referred to as barometric pressure = P b)

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26
Q

What is the alveolar pressure symbol?

A

P alv (or PA)

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27
Q

What is P ip?

A

Intra pleural pressure

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28
Q

What is P tp?

A

Transpulmonary pressure (or lung pressure PL)

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29
Q

What is P Ip (intra pleural pressure) at rest?

A

-4 mm Hg

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30
Q

What is atmospheric pressure?

A

0 mm Hg (all other respiratory pressures are a measure relevant to P atm).

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31
Q

What direction does air move?

A

By bulk from a region of high pressure to low pressure

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32
Q

What is bulk flow (F) proportional to?

A

Pressure difference

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33
Q

What is Bulk Flow (F) inversely proportional to?

A

Resistance (R)

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34
Q

What is the equation for bulk flow?

A

F = change in P / R

Change in P = (P alv - P atm)

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35
Q

At rest what is the difference between alveoli and atmosphere?

A

Zero

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36
Q

What are pressures in the respiratory system relative to?

A

Atmospheric pressure (at 760 mmHg)

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37
Q

What is flow when there is no pressure gradient?

A

0

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38
Q

What is Boyle’s law?

A

At constant temperatures the volume of a gas varies inversely with absolute pressure.

E.g., In the lungs volume increases and pressure decreases (in proportion to outside pressure). When volume decreases pressure has increases inside.

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39
Q

Does volume of the lung increase or decrease with inspiration?

A

Increase (therefore decreased pressure)

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40
Q

If lung volume increases what happens to pressure?

A

it decreases (volume and pressure inversely proportional)

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41
Q

What are the 2 determinants for the changes in lung dimension?

A

1) difference in the pressure between the inside and outside of the lung (transpulmonary pressure)

2) stretchability of the lungs (compliance) - how much the lungs can expand for a given change in transpulmonary pressure

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42
Q

What is the normal value for P tp?

A

4mmHg = the difference between 0 for P atm and -4 for P alv

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43
Q

What does transmural pressure resist?

A

The elastic recoiling of the lung (prevents the lungs from collapsing)

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44
Q

Does transmural pressure need to be positive or negative?

A

Needs to be positive so that the lungs press towards the lower pressure preventing them from collapsing.

If the value is negative the lungs would want to press inwards.

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45
Q

P alv - P ip gives us what value?

A

P tp

normally +4 because 0 - (-4)

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46
Q

When do lungs assume their smallest size?

A

When P tp is at zero

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47
Q

What is opposed when Ptp is positive?

A

Elastic recoil

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48
Q

What does Pip need to be in order for Ptp to be positive?

A

P ip needs to be negative

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49
Q

What is pneumothorax?

A

When air is in the pleural cavity e.g., the space between lung and chest wall (due to there being a collapsed lung)

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50
Q

What is a collapsed lung referred to?

A

Atelectasis

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51
Q

What is pleural effusion?

A

fluid in the pleural cavity

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52
Q

Is inspiration or expiration passive?

A

Expiration = passive
Inspiration = active

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53
Q

What nerves are activated during inspiration?

A

Intercostal nerve (located within ribs)
Phrenic nerve (located on top of diaphragm)

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54
Q

What occurs in the stages between the diaphragm and inspiratory intercostal muscles contracting and air flowing into the alveoli?

A

The thorax expands > Pip becomes more subatmospheric > increase in transpulmonary pressure > lungs expand > P alv becomes subatmospheric

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55
Q

What does ‘subatmospheric’ mean?

A

Lower than atmospheric pressure

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56
Q

What occurs in the stages between when the diaphragm/inspiratory intercostal muscles stop contracting and air flowing out of the lungs?

A

Chest wall recoils inwards > P ip moves back towards preinspiration value > transpulmonary pressure moves back towards preinspiration value > lungs recoil towards preinspiration size > air in alveoli becomes compressed > P alv become greater then P atm

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57
Q

What work needs to be done to breath?

A

1) overcome elastic properties (or stiffness) of the lungs

2) overcome airway resistance (friction)

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58
Q

What are the two elastic properties of the lungs?

A

Compliance and surfactant

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59
Q

What is lung compliance (CL)?

A

A measure of elastic property of the lung

Compliance is the inverse/opposite of stiffness

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60
Q

What is the equation for CL?

A

Lung compliance = change in lung volume / change in transpulmonary pressure

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61
Q

What does the compliance curve look like?

A

There are two curves: the inspiratory compliance curve and the expiratory compliance curve.

The inflation/expiratory curve is lower and the deflation/inspiratory curve loops overtop.

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62
Q

What is on the Y and X axis of the lung compliance graph?

A

X = P tp
Y = Lung volume

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63
Q

What are the two determinants of lung compliance?

A

(1) Stiffness/elasticity of the lung
(2) Surface Tension

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64
Q

If there is low compliance what does this mean about stiffness of the lungs?

A

Low compliance = stiff lungs and therefore the lungs need to do more work to expand

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65
Q

Is emphysema or fibrosis used to describe stiff lungs?

A

Fibrosis

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66
Q

What is Emphysema?

A

“Floppy” lungs due to high compliance.

It means that inspiration is easy because they are very stretchy and can increase in volume but means that expiration is difficult and requires more energy because there is low elastic recoil.

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67
Q

What is Fibrosis?

A

“Stiff” lungs due to low compliance.

It means that inspiration is difficult and requires more energy because lungs are not stretchy but means that no additional energy is required for expiration because there is high elastic recoil.

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68
Q

Where is surface tension and what causes it?

A

Attractive forces between water molecules pulling together creates high surface tension at the fluid gas interface (surface of alveoli)

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69
Q

What effect does surfactant have on surface tension?

A

It reduces surface tension in alveoli = makes them easier to expand.

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70
Q

What is surfactant produced by?

A

alveolar type 2 cells called pneumocytes

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71
Q

What are pneumocytes?

A

Alveolar type 2 cells that produce surfactant

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72
Q

What is the major constituent of surfactant?

A

Phospholipids

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73
Q

How does surfactant lower surface tension?

A

Reduces attractive forces between fluid molecules lining the alveoli (fluid-gas interface) therefore there is a reduction in surface tension of alveoli and thus easier to increase lung size (increased compliance).

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74
Q

What is the result of a lack of or failure to produce adequate surfactant?

A

Stiff lungs

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75
Q

When is surfactant absent?

A

Absent in premature infants - therefore is a baby is born prior to 28 weeks it results in RDS (respiratory distress syndrome).

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76
Q

How is newborn RDS treated?

A

Assisted ventilation and administration of natural or synthetic surfactant given through the infants trachea (why premature born babies go into ICU)

RDS = respiratory distress syndrome

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77
Q

What is laminar flow and when does it occur in relation to breathing?

A

During quiet breathing flow in laminar meaning that it is smooth and regular.

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78
Q

What is resistance to flow determined by (law and equation)?

A

Poiseuille’s Law

R = 8nI / pie r^4

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79
Q

What is asthma?

A

Bronchoconstriction / bronchodilation and their effects on resistance and thus airflow

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80
Q

What is the main area of airway resistance?

A

Bronchi

(the first 6 generations of the airway)

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81
Q

Is resistance higher in smaller or larger respiratory airways and why?

A

Larger because resiatcne depends on the number of parallel pathways present (whereas in vascular system arterioles are arranged in series so has opposite effect).

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82
Q

What is radial traction?

A

The pulling of adjacent alveoli which reduces airway resistance

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83
Q

What are the diseases caused by airway resistance?

A

Asthma

Chronic obstructive pulmonary disease (COPD)

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84
Q

What are the two types of COPD?

A

COPD = chronic obstructive pulmonary disease

Emphysema
Chronic Bronchitis

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85
Q

What can you assess through a pressure-volume loop?

A

Pressure-Volume loop gives information on compliance of lungs (work of breathing).

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86
Q

Why is expiration passive?

A

Because you have already done the work by stretching the lungs during inspiration and the lungs elastic recoil does the work during expiration

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87
Q

What is a restrictive lung disease?

A

Problem with stretch/stiff lung

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88
Q

How is the pressure-volume curve changed when lung compliance decreases?

A

Shifted to the right

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89
Q

In an obstructive lung disease how is airway resistance affected?

A

It is increased

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90
Q

What is PEFR?

A

Peak Expiratory Flow Rates

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91
Q

What is the most common pulmonary function test?

A

Spirometry - measures lung volumes and air flow rates (measuring how much and how fast)

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92
Q

What is tidal volume?

A

Volume of air moved in and out of the lungs during normal quiet breath.

Approx. 500 ml

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93
Q

What is inspiratory reserve volume?

A

Biggest breath in

Extra volume that can be inspired with maximal inhalation (by using external intercostal muscles).

Approx. 3L

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94
Q

What is expiratory reserve volume?

A

Biggest breath out

Extra volume that can be exhaled with maximal effort (internal intercostal and abdominal muscles).

Approx. 1.2L

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95
Q

What is residual volume?

A

Volume remaining in the lungs after maximal exhalation (max breath out).

Approx. 1.2 L

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96
Q

What is inspiratory capacity?

A

Maximal breath in

Tidal volume + inspiratory reserve volume.

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97
Q

What is vital capacity?

A

Maximal breath in and out. Volume of air can shift in/out of lungs.

Inspiratory reserve volume + tidal volume + expiratory reserve volume.

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98
Q

What is function residual capacity?

A

Remaining volume at end of normal breath out when there is no inspiratory or expiratory muscle contractions.

Residual volume + expiratory reserve volume

Approx. 2.4L (40% TLC)

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99
Q

What is total lung capacity?

A

Total volume in lungs when maximally full

Approx. 6L

All volumes added together (tidal volume + inspiratory reserve volume + expiratory reserve volume + residual volume).

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100
Q

What is the importance of a large FRC?

A

At all times during the breath cycle O2 and CO2 exchange can occur between alveolar gas and the pulmonary capillaries.

It prevents fluctuation in the composition of alveolar gas.

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101
Q

What is restrictive lung disease?

A

Lung state that requires increased work due to decreased lung compliance = “stiff lungs”.

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102
Q

How does breathing change with restrictive lung disease?

A

You breath more shallowly and rapidly

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103
Q

What is obstructive lung disease?

A

Lung state where there is increased work due to airway resistance = narrow pipes

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104
Q

How does breathing change when you have obstructive diseases?

A

Breath more slowly and deeply

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105
Q

What do forced measurements give information about?

A

About air flow rates.

FEV1/FVC ratio used for distinction between obstructive and restrictive lung diseases.

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106
Q

What is forced vital capacity (FVC)?

A

The maximum breath into maximum breath out - force your breath out as hard as possible

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107
Q

What is FEV1?

A

The forced expiratory volume in one second

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108
Q

In healthy lungs approximately what percentage of lung volume is expirated in 1 second?

A

80%

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109
Q

If FEV1/FVC ratio is less than 70% what does it suggest?

A

Obstructive lung disease

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110
Q

How does the FEV1/FVC ratio change for restrictive lung disease?

A

The ratio doesn’t change because there is no change in airway resistance.

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111
Q

What are examples of obstructive lung disease?

A

Emphysema
Asthma

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112
Q

What is an example of restrictive lung disease?

A

Fibrosis

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113
Q

How do you work out total mouth ventilation?

A

frequency (breaths per minute) x tidal volume (ml per breath)

Units in ml/min

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114
Q

How many breaths do we approximately take per minute (breathing rate/frequency)?

A

10-12

115
Q

How do you convert ml to L?

A

divide by 1000

116
Q

In what circumstances does Ve (total mouth ventilation) change?

A

Either involuntarily in order to match metabolic demands or voluntarily due to consciously changing breath behaviour

117
Q

What is dead space ventilation (VD)?

A

The proportional of inhaled air that never gets to the alveoli so cannot be used for gas exchange.

118
Q

What are the two types of dead spaces contributing to VD value?

A

1) Anatomical dead space
2) Physiological/Functional dead space

VD = anatomical + functional

119
Q

Where is anatomical dead space mainly located?

A

Large conducting airways which includes the tranche, bronchi and noinrespiratory bronchioles.

120
Q

Where is functional dead space located?

A

Smaller respiratory areas including respiratory bronchioles and alveolar ducts.

121
Q

Approximately how much of inspired air is dead space?

A

1/3rd = 150ml

122
Q

Of the 150ml of dead space how much is in the anatomical dead space and how much is in the functional dead space?

A

Anatomical = 145ml
Functional = 5ml

123
Q

If you know the dead space what does it allow you to calculate?

A

alveolar ventilation (Va)

124
Q

How is dead space used as a diagnostic tool for pulmonary fibrosis and pulmonary hypertension?

A

Pulmonary Fibrosis - increases dead space by transforming respiratory tissue into fibrotic tissue

Pulmonary hypertension - increased dead space by impairing pulmonary perfusion (pulmonary arteries not function properly)

In both cases respiration is impaired and this also affects ventilation.

125
Q

What is hyperventilation?

A

Increased breathing rate

126
Q

What is hypoventilation?

A

Decreased breathing rate

127
Q

What else is induced from hypoventilation?

A

Hypoxia because you are bringing less oxygen in and hypercapnia because there is an increase in CO2.

128
Q

What else is induced from hyperventilation?

A

Hyperoxia because bringing in more oxygen and hypocapnia because there is a decrease in CO2.

129
Q

Is gas exchange high during fast shallow breathing or slow deep breathing?

A

Slow deep breathing

130
Q

How do you quantify individual atmospheric gases?

A

Partial Pressure

131
Q

What is Dalton’s law equation?

A

Partial Pressure = fraction of individual gas x total gas exchange

132
Q

What does a dot abbreviation mean?

A

Rate

133
Q

What is F?

A

Fractional concentration of a gas

134
Q

What is Dalton’s law of partial pressure?

A

In a gas mixture (air), each gas exerts its own individual pressure, called a partial pressure (P), in direct proportion to its fractional concentration in the mixture.

135
Q

How do you work out a fractional concentration?

A

……. Divide by 100

136
Q

What is the partial pressure of O2 on the summit of Mt Everest?

A

253 mmHg

137
Q

What is the partial pressure of O2 on the summit of Mt Aoraki?

A

487mmHg

138
Q

What happens to the temperature of air as it moves down the respiratory tract?

A

Warmed

139
Q

What does a change in the ratio of ventilation to perfusion impair?

A

Impairs O2 and CO2 transfer

140
Q

What is the normal ratio of ventilation to perfusion?

A

0.8

141
Q

What is alveolar ventilation in a healthy lung?

A

4L/min

142
Q

What is pulmonary blood flow in a healthy lung?

A

5L/min

143
Q

What are examples of lung diseases where there is a mismatch in the ratio of ventilation to perfusion due to ventilation being impaired?

A

Atelectasis (fibrosis), emphysema, pulmonary oedema (fluid).

144
Q

What are examples of vascular diseases where there is a mismatch in the ratio of ventilation to perfusion due to perfusion being impaired?

A

Pulmonary hypertension
Heart failure
Vascular disease associated with COPD

145
Q

What are the different names for the alveoli blood barrier?

A

Air-blood barrier
Blood-gas barrier
Alveocapillary membrane

146
Q

How do gases move across the alveolar capillary membrane?

A

By diffusion

147
Q

What is the diffusion of gases directly proportional to (Fick’s law)?

A

Surface area
Diffusion constant
Pressure difference

148
Q

What is the diffusion of gases inversely proportional to (Ficks law)?

A

Thickeness

149
Q

What does Fick’s law of diffusion explain?

A

Explains gas exchange through the membrane

150
Q

What is the Fick’s law of diffusion equation?

A

F = A/T x D (P1-P2)

(F = Flux = amount flowing)

151
Q

What does the diffusion constant (D) of Fick’s law of diffusion depend on?

A

Graham’s law = depends on gas solubility and its molecular weight

152
Q

On a per-molecular basis how much faster does CO2 diffuse than O2 and why?

A

20x faster and due to its higher solubility

153
Q

What is Emphysema?

A

A disease characterised by dilation of the alveolar spaces and destruction of the alveolar walls (essentially it is a reduction of SA reduces diffusion capacity).

154
Q

What is pulmonary fibrosis?

A

Involves thickening and scarring of the alveolar membranes (increases diffusion distances reduces the diffusion capacity)

155
Q

What can pulmonary fibrosis arise from?

A

Chronic inflammation, drugs, industrial chemicals

156
Q

What is pulmonary oedema?

A

Water accumulation in alveoli increase diffusion distance

157
Q

What is the main factor that influences Ficks law?

A

Pressure difference = gradient = because it is what drives diffusion

158
Q

What is the approximate alveolar partial pressure of oxygen?

A

100mmHg

159
Q

What three things does alveolar partial pressure of oxygen depend on?

A

1) PIO2 of inspired air
2) Alveolar ventilation
3) Oxygen consumption

160
Q

Why is it the balance between oxygen consumption and alveolar ventilation that is most important to alveolar partial pressure?

A

Because atmospheric PO2 is usually constant

161
Q

What is the alveolar partial pressure of carbon dioxide?

A

Kept constant at 40mmHg

162
Q

What 3 things does alveolar partial pressure of carbon dioxide depend on?

A

1) Alveolar ventilation
2) Carbon dioxide production
3) PICO2 of inspired air

163
Q

What is negligible in alveolar PACO2?

A

Atmospheric PICO2

164
Q

What are the 5 mechanisms that can cause arterial hypoxemia?

A

1) Reduced PB or FIO2
2) Hypoventilation
3) Impaired diffusion
4) Shunt
5) Ventilation-perfusion mismatching

165
Q

What causes hypoventilation?

A

Sleep

Morphine and barbiturates

Damage to the chest wall or paralysis of the respiratory muscles

High resistance to airflow - increased work of breathing

166
Q

What is RQ abbreviation for?

A

Respiratory Quotient

167
Q

What is Respiratory Quotient?

A

The amount of CO2 produced in relation to the amount of O2 consumed by metabolism (dependant on caloric intake).

168
Q

What is the RQ equation?

A

RQ = amount of CO2 excreted and produced divided by the amount of O2 taken up

169
Q

What is RQ for exclusive fatty acid metabolism?

A

0.7

170
Q

What is RQ for exclusive carbohydrate metabolism?

A

1.0

171
Q

What is RQ for normal dietary conditions?

A

0.8

172
Q

How is diffusion (Fick’s law) altered during exercise?

A

More capillaries are perfused (meaning more blood goes through capillaries)

Increased volume increases capillary surface area and reduces diffusion distance for capillaries.

173
Q

what are the two forms that oxygen is carried in the blood?

A
  1. Dissolved O2
  2. Combined with haemoglobin
174
Q

For every mmHg of PO2 how much is dissolved?

A

0.03 ml

175
Q

Arterial blood with PO2 of approximately 100 mmHg contains how much dissolved O2 per litre?

A

3 ml therefore 0.003 L

176
Q

Is dissolved O2 effective for oxygen transport?

A

No it is very ineffective

177
Q

How much oxygen do we need per a minute?

A

About 250 ml / min

178
Q

What is haemoglobin?

A

A protein complex:

4 heme + globin (4 peptides) = haemoglobin (Hb)

179
Q

How many subunits does haemoglobin have?

A

4

180
Q

What is a haemoglobin subunit known as?

A

Globin

181
Q

How many heme groups does one Hb protein have?

A

4 (1 heme group attached to each subunit).

182
Q

What does oxygen bind to in Hb protein?

A

The iron atom of the heme

183
Q

If you have a lack of iron what does it cause?

A

A form of anemia - Affects O2 binding / carrying capacity.

184
Q

How many oxygens can bind to a heme?

A

1

185
Q

What is formed when O2 binds to Hb?

A

Oxyhemoglobin (HbO2)

186
Q

Is Oxyhemoglobin reversible?

A

Yes - “Easily reversible”

187
Q

What determines blood colour?

A

Oxygen binding (therefore the heme group and its iron atom)

188
Q

Is oxygenated or deoxygenated blood more red?

A

Oxygenated (because has more Hb)

189
Q

If blood is black what does that mean?

A

That there is no O2 in the blood

190
Q

Is arterial or venous blood more red?

A

Arterial (because more oxygenated)

191
Q

what does binding of O2 depend on?

A

Partial pressure of O2

192
Q

What type of curve is the oxygen-haemologobin curve?

A

Sigmoidal NOT linear

193
Q

What is on the x and y axis of the oxygen-Hb graph?

A

x axis = partial pressure of oxygen in the blood

y axis = hemoglobin saturation (%)

194
Q

What is hemoglobin saturation?

A

The amount of O2 being loaded (e.g., the amount of O2 binded to Hb)

195
Q

Is haemoglobin saturation greater for systemic venous Po2 or systemic arterial Po2?

A

Arterial

196
Q

Is the oxygen-haemoglobin curve fixed?

A

No - if can shift left and right known as the Bohr effect

197
Q

What is systemic venous Po2?

A

40 mmHg

198
Q

What is systemic arterial Po2?

A

100 mmHg

199
Q

explain the upper flat part of the oxygen-Hb curve?

A

It shows that moderate changes in Po2 around the normal value have only small effects on the % saturation and therefore the amount of O2 carried by arterial blood = meaning there is some reserve capacity.

200
Q

Explain the steep part of the oxygen-Hb curve at lower Po2?

A

It shows that small changes in Po2 results in large changes in the amount of O2 bound to Hb. The more linear relationship at lower Po2 help with loading of Hb in lungs and unloading to the tissues.

201
Q

What is the maximal amount of O2 that can be combined with Hb called?

A

O2 carrying capacity (which is the amount of O2 carried when Hb is 100% saturated).

202
Q

One gram of Hb can typically combine with how much O2?

A

1.34 ml of O2

203
Q

Normal blood has about how much Hb per litre?

A

150 g Hb / litre

204
Q

How do you work out the O2 content of the blood ignoring any dissolved oxygen?

A

1.34 x Hb x saturation/100

205
Q

How do you work out the O2 content of the blood?

A

(1.34 x Hb x sat/100) + 0.03 x PaO2

O2 content of the blood = O2 capacity + O2 dissolved

206
Q

How do you work out the amount of O2 extracted by tissues?

A

Arterial - venous O2 difference = amount of O2 extracted by tissues

207
Q

If the a - v difference is 50 ml O2/litre blood what exactly is it telling us?

A

That 50ml of o2 is extracted from each litre of blood by the tissues and used in metabolism

208
Q

What provides the capacity for more oxygen to be extracted and used by tissues when exercising?

A

initially the reserve capacity

209
Q

What is the Bohr effect?

A

the principle that the oxygen-haemoglobin curve can shift left or right

210
Q

Explain a left shift of the O-Hb curve?

A

Left shift = loading/onloading

A left shift in the curve represents the improved loading of O2 by Hb due to an increase in O2 affinity facilitating the uptake of O2 from the alveoli into the blood.

211
Q

What is decreased in a left shift in curve?

A

PCO2 and therefore H+ Temperature
2,3 DPG

212
Q

When does a natural left shift occur?

A

As blood flows through the lung capillaries

213
Q

What is a right shift of the O2-Hb curve?

A

Right shift = release / offloading

It is the favouring of releasing O2 from Hb to the tissues - right shift improves the delivery of O2 by Hb.

214
Q

What is increased in a right shift of the curve?

A

PCO2, H+, Temperature and 2,3 DPG

215
Q

What is 2,3 DPG a by product of?

A

Glycolysis

216
Q

Do RBC have mitochondria?

A

No (therefore they rely on glycolysis)

217
Q

What is glycolysis?

A

The breakdown of glucose by enzymes, releasing energy (ATP) and pyruvic acid (anerobic metabolism).

218
Q

When does 2,3 DPG increase?

A

intense exercise training, altitude and due to severe lung diseases or anemia

219
Q

What does 2,3 DPG help do?

A

helps deliver O2 to tissues

220
Q

What is the effect of anaemia on the O2 saturation curve?

A

Anemia (which is low RBC therefore HB and therefore oxygen carrying capacity) does not affect the saturation curve.

221
Q

What is CO?

A

Carbon monoxide

222
Q

Does CO (carbon monoxide) have a high or low affinity to Hb?

A

High - around 250 times the affinity of O2 for Hb

223
Q

What is the effect of CO (carbon monoxide)?

A

it decreases O2 content in the blood because it binds to the Hb preventing O2 from binding.

224
Q

What causes an increase in arterial CO?

A

Smoking

225
Q

What are the three forms that CO2 can be transported in?

A
  1. Dissolved in plasma (10%)
  2. As bicarbonate (70%)
  3. Combined with proteins as carbamino compounds (20%)
226
Q

Is oxygen or carbon dioxide more soluble?

A

Co2

227
Q

What dissociates to form Bicarbonate?

A

Carbonic acid broken down into hydrogen ion and bicarbonate ion

Carbonic acid is very unstable so immediate dissociates.

228
Q

What is the Haldane effect?

A

The upwards or downwards shift of Co2-blood dissociation curve

229
Q

Explain an upwards shift of the Co2-blood dissociation curve:

A

Co2 and H+ bind more readily to goblin chain when the heme contains less O2.

I.e., as arterial blood flows through the tissue capillaries losing O2, the change in molecular configuration of Hb favours the loading of Co2 onto the globin chain.

230
Q

Explain a downwards shift in Co2-blood dissociation curve:

A

CO2 and H+ bind less readily to goblin chain when the heme contains more O2.

i.e., as venous blood flows through the lung capillaries gaining O2, the change in molecular configuration of Hb to promote the release of CO2 in the alveoli.

231
Q

Is the CO2-blood curve or the O2-Hb curve more linear?

A

Co2-blood

232
Q

Where does O2 enter the blood RBC?

A

Lung alveoli

233
Q

Where does CO2 enter blood RBC?

A

Peripheral tissues

234
Q

What is the chloride shift?

A

A chloride shift exchanges bicarbonate (HCO₃⁻) for chloride ions (Cl⁻) to maintain charge balance.

235
Q

What is respiration a combination of?

A

Brain, chest wall and lungs

236
Q

What are the three basic elements for the control of breathing?

A
  1. central controller
  2. effectors
  3. sensors
237
Q

What are the central controllers of breathing?

A

Midbrain pons and medulla and some other parts of the brain

238
Q

What are the effectors of breathing?

A

Respiratory muscles

239
Q

What do the central controllers of breathing do?

A

Set pattern/rhythm of breathing to coordinate sensors and effectors to maintain respiratory homeostasis

240
Q

What do the effectors of breathing do?

A

Adjust ventilation

241
Q

What are the sensors of breathing?

A

Chemoreceptors, lungs and other receptors

242
Q

What do sensors of breathing do?

A

Receive a variety of neural and chemical inputs from central and peripheral receptors

243
Q

Where are the respiratory rhythmicity centres located in the brain?

A

Medulla oblongata

244
Q

Where are the apneustic and pneumotaxic centres located in the brain?

A

Pons

245
Q

What are the 3 respiratory rhythmicity centres?

A

Inspiratory centre of the dorsal respiratory group (DRG)

Ventral respiratory group (VRG)

Pre-Botzinger complex

246
Q

What is the respiratory rhythm generator?

A

Pre-Botzinger complex

247
Q

Where does the neurons of the DRG go to?

A

To diaphragm and to external intercostal muscles (for inhalation)

248
Q

Where do the neurones of the VRG go to?

A

Inspiratory neuron’s to accessory inspiratory muscles

Expiratory neuron’s to accessory expiratory muscles

249
Q

What centres adjust the output of the respiratory rhythmicity centres?

A

Pneumotaxic and apneustic centers

250
Q

What is the pneumotaxic centre also known as?

A

Pontine respiratory group (PRG)

251
Q

What can higher centers of respiratory control do?

A

Can alter the activity of the pneumotaxic centers

(They can override everything)

252
Q

What are the three higher centers of respiratory control?

A

Cerebral cortex
Limbic system
Hypothalamus

253
Q

What do chemoreceptors respond to?

A

Change in the chemical composition of blood or other fluid surrounding it

254
Q

What are the chemicals in the respiratory system?

A

CO2
O2
H+
HCO3-

255
Q

What are the two types of chemoreceptors?

A

Central chemoreceptors
Peripheral chemoreceptors

256
Q

What chemicals act mainly through peripheral chemoreceptors?

A

O2 and H+ (H+ that is not due to CO2)

257
Q

What are central chemoreceptors?

A

Specialised cells on the ventrolateral surface of the medulla (located in medulla oblongata)

258
Q

What are central chemoreceptors sensitive to?

A

Changes in the partial pressure of arterial CO2 (PCO2). Therefore sensitive to hypocapnia and hypercapnia.

Also sensitive to changes in pH in brain extracellular fluid as a result of increases H+ concentrations (NOT arterial acidity)

259
Q

What are central chemoreceptors not sensitive to?

A

PaO2
Arterial acidity

260
Q

What do central chemoreceptors activate in the brain?

A

DRG (inspiratory center)

261
Q

Is carbon dioxide permeable to the blood brain barrier?

A

Yes - CO2 is easily diffusible across the blood brain barrier.

262
Q

What is hypercapnia and hypocapnia?

A

Abnormal levels of CO2 in the blood

Hyper = high blood CO2
Hypo = low blood CO2

263
Q

What percentage of the increase in ventilation is a result of central chemoreceptors activating DRG?

A

Around 70%

264
Q

What are peripheral chemoreceptors closely related to?

A

Arterial baroreceptors

265
Q

What are peripheral chemoreceptors sensitive to?

A

Changes in the partial pressure of arterial O2 (PaO2) therefore hypoxia and hyperoxia.

And arterial acuity due to increased H+ concentration (this change in H+ ion is not due to Co2 but instead metabolic acidosis such as lactic acid).

And less significantly by an increased PCo2 (respiratory acidosis / changes in partial pressure of alveolar CO2).

266
Q

What is the predominant peripheral chemoreceptor?

A

Carotid bodies

(but they are also in aortic bodies)

267
Q

Why is the major stimuli for the increased ventilation at moderate exercise NOT due to an increase in Co2 production?

A

Exercising muscles produce more CO2 - but this increases only venous PCO2 and not arterial PCO2 because the level of PCO2 is determined by alveolar PCO2 which is determined by the ratio of CO2 production and alveolar ventilation - both of these things increase with exercise therefore there is no change (arterial PCO2 is kept constant).

268
Q

Total oxygen transport by the blood is not reduced very much until the arterial PO2 falls below what?

A

60 mmHg (sigmodial curve)

269
Q

At what point does increased ventilation result in more oxygen being added to the blood?

A

60 mmHg

270
Q

What are three physiological changes that occur when you acclimatise to high altitude?

A

1) Increased erythrocyte and haemoglobin therefore oxygen carrying capacity in the blood

2) Increased oxygen transfer due to increased skeletal muscle capillary density, mitochondria and muscle myoglobin.

3) Decreased plasma volume

271
Q

What does a decreased plasma volume result in?

A

Increased concentration of the erythrocytes and haemoglobin in the blood

272
Q

How does skeletal muscle capillary density increase in high altitude?

A

Under normal conditions not all capillaries are opened - when in altitude hypoxia can stimulate the opening and production of more capillaries by inducing the expression of the gene that codes for angiogenic factor.

As a result you can bring in more blood and thus more oxygen to tissues.

273
Q

What is erythropoietin?

A

A hormone secreted primarily by the kidney that stimulates erythrocyte synthesis (RBC production)

Produced in kidney and can be stored in bone marrow.

274
Q

What prevents even small increases in arterial PCO2?

A

Reflex mechanisms controlling ventilation

275
Q

What is commonly seen in emphysema?

A

Reflex mechanisms controlling ventilation

276
Q

What is Respiratory acidosis ?

A

Respiratory acidosis is when your lungs can’t remove all the carbon dioxide that your body produces, so your blood pH is lower (more acidic) than normal.

277
Q

What is Respiratory alkalosis ?

A

Respiratory alkalosis is when hyperventilation causes low carbon dioxide levels, so your blood pH is higher (more basic) than normal.

278
Q

What is metabolic acidosis?

A

A build up of acid in the body. Occurs during anaerobic metabolism as lactic acid is created as a by product during exercise

279
Q

What is metabolic alkalosis?

A

A loss of H+

Can occur due to vomiting.

280
Q

What is the normal human physiological pH?

A

Normal human physiological pH is 7.35 to 7.45.

A decrease in pH below this range (less than 7.35) is acidosis, an increase over this range (more than 7.4) is alkalosis.

281
Q

If there is a decrease in arterial PO2 what happens in order to increase ventilation?

A

Increase in peripheral chemoreceptor firing.

Increase in firing of medullary inspiratory neuron’s

Increase in firing of neurones to diaphragm and inspiratory intercostals

Increase in contractions of diaphragm and inspiratory intercostals

Increase in ventilation

282
Q

What happens when there is an increase in arterial H+ in order to return it towards normal levels?

A

Increased firing of peripheral chemoreceptors - reflex via medullary report neuron’s

Increase in contraction of respiratory muscles

Increased ventilation (pushing out CO2)

Decrease alveolar and arterial PCO2

= return of arterial H+ towards normal

283
Q

If there is an increase in arterial PCO2 what happens?

A

Increase CO2 and H+ in brain extracellular fluid causing increasing in firing of central chemoreceptors.

Increase in firing of medullary inspiratory neuron’s

Increase in firing of neurones to diaphragm and inspiratory intercostals

Increase in contractions of diaphragm and inspiratory intercostals

Increase in ventilation

284
Q

What volume cannot be measure with spirometer?

A

Residual volume