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Respiratory - Medicine 1 > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

4 functions of respiratory system

A
  1. gas exchange - O2 to blood from air, CO2 from blood to air
  2. Acid-base balance - regulation of body pH
  3. protections from infection - cilia/epithelial tissue?
  4. communication via speech
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2
Q

what 2 systems are required to deliver fuel to active cells within tissues and remove waste products

A

CVS and respiratory system

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3
Q

compare cellular (internal) to external respiration

A
  • Cellular - biochemical process releasing energy from glucose either via glycolysis or oxadative phosphorylation. Latter requires oxygen and depends on external respiration
  • External respiration: movement of gases beteen the air and the body’s cells via both the respiratory and CVS
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4
Q

compare function of pulmonary and systemic circulation

A

Pulmonary: Delivers CO2 to lungs and collects O2 from the lungs
Systemic: delivers O2 to peripheral tissues and collects CO2

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5
Q

what does pulmonary artery carry

A

deoxygenated blood

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6
Q

what does pulmonary vein carry

A

oxygenated blood

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7
Q

Give an example of the integration between the CV and respiratory systems

A

Inc energy demand but working muscle leads to:
Resp: inc rate and depth of breathing; speeding up a)substrate (O2) aquisition and b) waste disposal (CO2)
CV: Ince HR and force of contraction; speeding up a) substrate delivery to muscle via blood and b) waste removal via blood

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8
Q

what is the net volume of gas exchanged in the lungs per unit time

A

250ml/min O2 and 200ml/min CO2

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9
Q

what does the net volume of gas exchanged in the lungs per unit time equal?

A

the net volume exchanged in the tissues

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10
Q

what does; net gas exchange [lungs] = net gas exchange [tissues] prevent?

A

gas build up in circulation which would hamper gas exchange and helps ensure supply = demand

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11
Q

normal and excercising respiration rate

A

12-18 breaths/min - rest
40-45 at max exercising capacity in adults

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12
Q

what 2 levels are O2 and CO2 exchanged at

A

lungs, peripheral tissues

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13
Q

equation of life

A

Nutrients + O2 = Energy (ATP) + waste (incl. CO2)

(intracellular respiration)

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14
Q

7 parts of respiratory system

A

Nose: airs enters, cilia and mucus trap particles and warm/moisten air
Pharynx: air moves down into pharynx (throat) which is shared with digestive system
Epiglottis: small flap of tissue folds over trachea and prevents food from entering it when swallowing
Larynx: “voice box” containing vocal chords
Trachea: stiff rings of cartilage (support and protection)
Lung: soft, spongy texture due to thousands of tiny sacs (alveoli) that compose them
Bronchus: air moves from trchea to right and left bronchi which lead inside the lungs

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15
Q

parts of upper respiratory tract

A

mouth, nasal cavity, pharynx, larynx

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16
Q

parts of lower respiratory tract

A

trachea, bronchi, lungs

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17
Q

number of lobes in left/right bronchi

A

Left: 2 lobes
Right: 3 Lobes

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18
Q

how many secondary bronchi in left/right lungs

A

Left: 2
Right: 3

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19
Q

name parts of right lung

A
  • Superior lobe
  • —horizontal fissure
  • middle lobe
  • — oblique fissure
  • inferior lobe
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20
Q

name parts of left lung

A
  • superior lung
  • — oblique fissure
  • inferior lobe
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21
Q

pericardium

(heart related…)

A

a protective, fluid-filled sac that surrounds your heart and helps it function properly

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22
Q

conc gradient aka…

A

partial pressure gradient

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23
Q

explain branching of airways

A

trachea branches into 2 bronchi. Each bronchus branches 22 more, terminating in cluster of alveoli

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24
Q

how many times do the airways branch

A

24

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25
Q

parts of repiratory system showing patancy

A

larynx, trachea, bronchi (primary + secondary)

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26
Q

patancy

A

the condition of being open or unobstructed

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27
Q

what maintains patancy

A

semi-rigid tubes, patancy of airway is maintained by C-shaped rings of cartilage

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28
Q

order of branching within the lungs

A

bronchi, bronchioles, alvioli

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29
Q

bronchiole

A

no cartilage, patency maintained by physical forces in thorax

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30
Q

alveoli

A

point of gas exchange

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31
Q

conducting zone

A

all of the structures that provide passageways for air to travel into and out of the lungs: the nasal cavity, pharynx, trachea, bronchi, and most bronchioles

NOT alveoli

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32
Q

compare shape/size of bronchi

A

Right: larger/wider and more verticle

aspirated foreign bodies found more commonly here

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33
Q

respiratory zone

A

alveoli

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34
Q

where is there most resistance to air flow

A

in least branched areas (e.g. bronchi, trachea)

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35
Q

conducting vs respiratory zone

A

conducting zone is everything apart from place of gas exchange (alveoli) which is respiratory zone

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36
Q

what does air in the conducting zone sit in

A

dead space

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37
Q

what can be altered by activity of bronchial smooth muscle

A

airway diameter, and therefore resistance to airflow

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38
Q

explain relationship between bronchial contraction and resistance

A

contraction dec diameter = ince resistance
relaxation inc diameter = dec resistance

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39
Q

what is each cluster of alveolis surrounded by

A

elastic fibres and a network of capillaries

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40
Q

what doe elastic fibres allow for

A

expansion/contraction of alveoli during respiration

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41
Q

give a common pathology of elastic fibres

A

emphyseama

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42
Q

types of cells found in alveoli

A

Type 1: gas exchange
Type 2: synthesise surfactant

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43
Q

what other cell (not type 1 or 2) is found in alveolar structure

A

alveolar macrophages ingest foreign materil that reaches the alveoli

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44
Q

type 2 (surfactant cells)

A

produce surfactant so not involved in gas exchange

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45
Q

what are always directly abuted together

A

capilallary (endothelial) cells and type 1 cells - minimises diffusion distance for gas exchange

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46
Q

what is good about alveoli in terms of gas exchange

A

large surface area - 80m2

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47
Q

where is gas exchange between lungs and blood only possible

A

at alveoli: due to their thin surface

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48
Q

what do areas of the upper airways contain and why

A

anatomical dead space - unable to participate in gas exchange as the walls of the airways are too thick

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49
Q

airway resistance

A

how much air flows into the lungs at any given pressure defference between atmosphere and alveoli. Major determinant of airway resistance is the radii of the airways

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50
Q

approx vol. of lungs

A

6L

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51
Q

ventilation

A

air in/out of lungs (nothing to do with gas exchange)

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52
Q

lung volume/capacity diagram

A

see pic 1

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53
Q

dead space volume

A

150m volume of gas occupied by the conducting airways and not available for gas exchange

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54
Q

tidal volume

A

volume of air breathed in and out of the lungs at each breath

see pic 1

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55
Q

expiratory reserve volume

A

max vol of air which can be expelled from the lungs at the end of a normal expiration

see pic 1

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56
Q

inspiratory reserve volume

A

max vol of air which can be drawn into the lungs at the end of a normal inspiration

see pic 1

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57
Q

residual volume

A

volume of gas in the lungs at the end of a maximal expiration

see pic 1

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58
Q

vital capacity

A

TV + IRV + ERV

see pic 1

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59
Q

total lung capacity

A

VC + RV

see pic 1

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60
Q

Inspiratory capacity

A

TV + IRV

see pic 1

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61
Q

functional residual capacity

A

ERV + RV

see pic 1

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62
Q

FEV1:FVC

A

fraction of forced vital capacity expired in 1 second

see pic 1

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63
Q

what is each lung enclosed in

A

2 pleural membranes (containing pleural fluid)

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64
Q

where do the esophagus and aorta pass through the thorax

A

between the pleural sacs

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65
Q

viscelral pleura

A

lung-side membrane

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66
Q

parietal plaura

A

more superficial membrane (attached to rib cage and diaphragm)

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67
Q

what are the lungs and interior of the thorax covered by

A

pleural membranses with extremely thin layer of pleural fluid between the membranes

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68
Q

what do the pleural membranes allow for

A

movement of lungs and rib-cage (during expansion/contraction) in a friction-free mannar

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69
Q

what effectively happen to the lungs through the relationship of the pleural membranes

A

they are stuck to the rib cage

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70
Q

function of pleural membranes

A

to stick the lungs to the rib cage

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71
Q

what is visceral pleura stuck to

A

surface of the lungs

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72
Q

how is the visceral pleura stuck to the parietal pleura

A

via the cohesive forces of the pleural fluid

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73
Q

what is the parietal pleura stuck to

A

the rib cage and diaphragm

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74
Q

explain lung expansion/contraction in relation to the pleural cavities

A

The lungs are effectively stuck to the rib cage and diaphragm and will follow the movements of these bones and muscles as the chest wall expands during inspiration.
The chest wall therefore leads the expansion of the lung during inspiration. In contrast, the elastic connective tissue in the lung leads to recoil of the chest wall in (unforced) expiration.

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75
Q

what is intrapleural pressure always

A

negative (subatmospheric)

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76
Q

what does negative intrapleural pressure prevent

A

collapsed lung (pneumothorax)

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77
Q

what happens to much of the lung capacity and when may it be used

A

not utilised during relaxed breathing at rest (tidal volume) but this “spare” capacity is vital and is utilised during periods of greater energy demand eg. exercise

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78
Q

what is the air imposible to remove from the lungs called

A

residual volume

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79
Q

what could be used to descibe the action of the pleural fluid

A

cohesive

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80
Q

how are the lungs stuck to, and expanded by the chest wall

A

by pleural membranes

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81
Q

what does recoil of the elastic connective tissue in the lungs bring about

A

recoil of the chest wall in normal expiration (although chest wall may be employed during forced expiration)

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82
Q

boyle’s law

A

pressure exerted by a gas is inversely proportional to its volume

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83
Q

what allows breathing to occur

A

the thoracic cavity changing volume

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84
Q

based off Boyle’s law how does inc/dec vol. affect pressure in the lungs/during breathing

A

Inc vol = dec pressure
dec vol = inc pressure

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85
Q

along what gradient do gases move

A

from high pressure to low pressure

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86
Q

what muscles are used during inspiration

A

external intercostal muscles and diaphragm

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87
Q

what muscles are used by expiration

A

is passive at rest but uses internal intercostal and abdominal muscles during severe respiratory load

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88
Q

give moredetailed list of muscles used for inspiration

A

diaphragm, external intercostals, sternocleidomastoids and scalenes

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89
Q

what muscles could be used in expiration

A

internal intercostals and the abdominals

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90
Q

describe movements of diaphragm during inspiration and expiration

A

Inspiration: contracts, thoracic volume inc
Expiration: relaxes, thoracic volume dec

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91
Q

what nerve innervates the diaphragm

A

phrenic nerve

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92
Q

bucket tap thinngy?

A

idea ribs move up and out when breathing and sternum moves up and down but also a little out

(plueral cavity then pulls lungs out too)

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93
Q

summarise the mechanics of breathing for inspiration and expiration

diaphragm motion, effect on vol, effect on airways, resistance to breath

A

Inspiration: Diaphragm contracts, thoracic vol inc, airways pulled open by physical forces of inspiration, least resistance to breathing
Expiration: diaphragm relaxes, thoracic vol dec, airways compressed by physical forces of expiration (aggravates asthma), most resistance to breathing

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94
Q

Intra-thoracic (alveolar) pressure (Pa)

A

pressure inside the thoracic cavity (essentially pressure inside lungs). Can be negative or positive compared to atmospheric pressure

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95
Q

Intra-pleaural pressure (Pip)

A

pressure inside the pleural cavity, typically negative

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96
Q

Transpulmonary pressure (Pt)

A

difference between alveolar pressure and intra-pleural pressure. Almost always positive because Pip is negative (in health)

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97
Q

good equation to knwo for common pressures…

A

Pt = Palv - Pip

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98
Q

why is intrapleural pressure negative

A

help maintain proper inflation of the lungs and to help prevent a pneumothorax (i.e. collapsed lung)

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99
Q

(mechanical?) factors to affect breathing

bit of a long one… confusion?

A
  • Bulk flow of air between the atmosphere and alveoli is proportional to the difference between the atmospheric and alveolar pressures and inversely proportional to the airway resistance: F = (Patm- PA)/R
  • Between breaths at the end of an unforced expiration Patm= PA, no air is flowing, and the dimensions of the lungs and thoracic cage are stable as the result of opposing elastic forces. The lungs are stretched and are attempting to recoil, whereas the chest wall is compressed and attempting to move outward. This creates a subatmospheric intrapleural pressure and hence a transpulmonary pressure that opposes the forces of elastic recoil
  • Airway resistance determines how much air flows into the lungs at any given pressure difference between atmosphere and alveoli. The major determinant of airway resistance is the radii of the airways
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100
Q

what kind of word could be used to describe lung structure

A

elastic

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101
Q

What does the lung’s volume depend on

A

the pressure difference actross the lungs (transpulmonary pressure) and how stretchable the lungs are

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102
Q

summarise the changes in pressure during inspiration and expiration

A

During inspiration, the contractions of the diaphragm and inspiratory (external) intercostal muscles increase the volume of the thoracic cage.
This makes intrapleural pressure more subatmospheric (negative) and causes the lungs to expand.
This expansion makes alveolar pressure subatmospheric, which creates the pressure difference between atmosphere and alveoli to drive air flow into the lungs.
During expiration, the inspiratory muscles cease contracting, allowing the elastic recoil of the chest wall and lungs to return them to their original between-breath size.
This compresses the alveolar air, raising alveolar pressure above atmospheric pressure and driving air out of the lungs.

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103
Q

what happens in terms of pressure in forced expiration

A

In forced expirations, the contraction of expiratory (internal) intercostal muscles and abdominal muscles actively decreases thoracic dimensions, reducing duration of breathing cycle and allowing more breaths/min

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104
Q

why is intrapleural pressure always less than alveolar pressure

A

intrapleural pressure pulls harder and harder on lungs to expand them. Alveolar pressure get negative the back to 0 on inspiration, then get positive and back to 0 on inspiration. Basically air catches up… equilibrium! :)

See pic 2

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105
Q

what is the natural tendancy of the lungs

A

to recoil (contract inwards)

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106
Q

surfactant

what is it, function

A

detergent like fluid produced by alveolar cells
Reduces surface tension on alveolar surface membrane thus reducing tendency for alveoli to collapse

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107
Q

what is surface tension and when does occur

A

the attraction between water molecules and occurs where ever there is an air-water interface

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108
Q

function of surfactant

A

Reduces surface tension on alveolar surface membrane thus reducing tendency for alveoli to collapse

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109
Q

what effects does surfactant have

A
  • inc lung compliance/distensibility
  • reduces lung’s tendancy to recoil
  • makes work of breathing easier
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110
Q

compliance

A

how easy it is to stretch lungs open

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111
Q

where is surfactant more effective and why

A

iin small alveoli than large alveoli because surfactant molecules come closer together and are therefore more concentrated

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112
Q

what cells produce surfactant

A

type 2 alveolar cells

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113
Q

give time-line of surfactant production… and what can happen to premature babies…

A

Surfactant production starts ~25 weeks gestation. Complete by ~36 weeks. (40 weeks = full term). Stimulated by thyroid hormones and cortisol which increase towards end of pregnancy.

Premature babies suffer Infant Respiratory Distress Syndrome (IRDS).

114
Q

inflation curve with air vs saline (like in IRDS?)

A

See pic 3

115
Q

compliance

A

change in volume relative to change in pressure - stretchability of lungs, not elasticity

116
Q

High compliance vs low compliance

+ when good/bad

A

High compliance = large inc in lung volume for small dec in ip pressure - only good if accompanied with high elasticity
Low compliance = small inc in lung volume for large dec in ip pressure - always bad

117
Q

what can compliance change with

A

disease states (e.g. fibrosis) and age (dec elastic function

118
Q

what, in part, determines compliance

A

action of surfactant (inc ease of expansion —> inc compliance)

119
Q

what determines compliance

A

elastic forces, surface tension at the alveolar air-liquid interface and by airway resistance

120
Q

does surfactant inc or dec compliance

A

inc compliance (but dec alveolar surface tension)

121
Q

where is surfactant more effective

A

in small alveoli

122
Q

law of laplace

A

Pressure is inversely proportional to the radius. The smaller the radius, the more pressure.

123
Q

what is anatomical dead space

A

volume of gas occupied by the conducting airways and not available for exchange
Roughly 150mL

124
Q

2 ways to describe ventilation

A

Pulmonary (minute) ventilation
Alveolar ventilation

125
Q

Pulmonary (minute) ventilation

A

total air movement into/out of lungs (relatively insignificant in functional terms)

126
Q

Alveolar ventilation

A

fresh air getting to alveoli and therefore available for gas exchange (functionally musch more significant)

127
Q

units for pulmonary and alveolar ventilation

A

L/min

128
Q

describe air that is gained and lost during inspiration and expiration (give volumes/quantities)

A

see pic 4

129
Q

average tidal volume

A

500mL

130
Q

normal respiratory rate

A

12-16 breaths/min

131
Q

what x what = pulmonary ventilation

A

respiratory rate + tidal volume

132
Q

terms for not enough/too much ventilation

A

hypoventilation, hyperventilation

133
Q

dalton’s law

A

the total pressure of a gas mixture is the sum of the pressures of the individual gases

134
Q

where does the CO2 in our cells/blood come from

A

us making it (and NOT breathing it in)

135
Q

define partial pressure

A

Pressure of a gas in a mixture of gases is equivalent to the percentalge of that particular gas in the entire mixture multiplied by the pressure of the whole gaseous mixture

136
Q

What can vary with hyper/hypo-ventilation

kinda key concept

A

Alveolar PO2 and PCO2

137
Q

What happens to PO2 and PCO2 during hyperventilation (inc alveolar ventilation)

A

PO2 rises to about 120 mmHg (from 100) and PCO2 falls to about 20mmHg (from 40)

138
Q

normal partial pressures of O2 and CO2

A

O2 = 100 mmHg (13.3 kPa)
CO2 = 40mmHg (5.3 kPa)

139
Q

what happens to PO2 and PCO2 during hypoventilation (dec alveolar ventilation)

A

PO2 falls to 30 mmHg and PCO2 rises to 100 mmHg

140
Q

why is normal PO2 at 100 mmHg and not atmospheric 160 mmHg

A
  • diluted by anatomical dead space and residual volume
  • saturated by water vapour so further diluted
  • is in equilibrium with pressure of gas in the blood
141
Q

what is Pgas in alveoli the same as

A

Pgas in systemic arterial blood

142
Q

what is the primary driving force for breathing and what does this make hard

in terms of gases

A

CO2: hard to hyperventilate

143
Q

why is CO2 the primary driving force for breathing

A

Is toxic so cells are sensitive to it/changes in [CO2]

144
Q

describe the pressure-volume curve and the discrepenceis between the base and the apex of the lung

learn - is confusing so maybe remake?

A

Varies:
* at base volume change is greater for a given change in pressure
* Alveolar ventilation declines with height from base to apex.
* Compliance is lower at the apex due to being more inflated at FRC. At the base the lungs are slightly compressed by the diaphragm hence more compliant on inspiration.
* A small change in intrapleural pressure therefore brings about a larger change in volume at the base compared with the apex

145
Q

describe relative alveolar ventilation and compliance at base vs apex of lung

A

Base: alveolar ventilation high, compliance low
Apex: alveolar ventilation low, compliance higher

146
Q

what would happen to pressure-volume curve if went from standing up to lying down

A

It would change - gravity has an effect

147
Q

Which type of ventialtion is functionally more important and what is it significantly influenced by

A

Alveolar ventilation (than pulmonary ventilation): anatomical dead space

148
Q

What is more influential at determening alveolar ventilation and why

A

Depth of breathing (than rate of breathing) - because of the effect of anatomical dead space

149
Q

what happens to alveolar ventilation as we move up the lung

A

declines with height from base to apex due to changes in compliance

150
Q

does hypo/hyper-ventilation alter partial pressures

A

yes

151
Q

what does the pulmonary artery carry

A

deoxygenated blood AWAY from the heart to the lungs

152
Q

what does the pulmonary vein carry

A

oxygenated blood TOWARDS the heart from the lungs

153
Q

what are the two kinds of blood supply to the lungs

A
  • bronchial circulation (nutritive)
  • Pulmonary circulation (gas exchange)
154
Q

bronchial circulation

A

nutritive: supplied via bronchial arteries arising from systemic circulation to supply oxygenated blood to lung tissues - 2% left heart output, blood drains to left atrium via pulmonary veins

155
Q

pulmonary circulation

A

gas exchange: consists of L and R pulmonary arteries originating from the right ventricle. supplies dense capillary network surrounding the alveoli and returns oxygenated blood to the left atrium via pulmonary vein. High flow, low pressure

156
Q

is pulmonary circulation in series or parrallel with systemic circulation

A

series

157
Q

A

A

alveolar

158
Q

a

A

arterial blood

159
Q

v

A

mixed venous blood (e.g. in pulmonary artery)

160
Q

partial pressures of O2/CO2 in alveolar/arterial/venous blood…

A

see pic 5

161
Q

what laws does gas exchange between alveoli and blood follow

A

simple diffusion - continues until equilibrium is reached

162
Q

what is the rate of diffusion across the membrane directly proportional to

A
  • partial pressure gradient
  • gas solubility (must be in solution to cross)
  • available surface area
163
Q

what is the rate of diffusion across the membrane inversely proportional to

A

the thickness of the membrane

164
Q

where is the rate of gas diffusion across the membrane most rapid

A

over short distances

165
Q

what does partial pressure in alveoli correspond with

A

PP in systemic arterial blood

166
Q

What does partial pressure in pulmonary arterial blood correspond with

(deoxygenated blood)

A

PP at tissues

167
Q

PP gradeint for O2 and CO2

A

PO2 = 100 —> 40 (250ml/min) alveoli to pulmonary artery
PCO2 = 46 –> 40 (200ml/min) pulmonary artery to alveoli

168
Q

what feature of the alveoli membrane allows for rapid diffusion

A

thin membrane so short diffusion distance

169
Q

what part of the heart is bronchial and pulmonary supple to the lungs each from

A

bronchial - left side (oxygenated blood)
pulmonary - right side

170
Q

what is pulmonary arterial pressure

A

low: 25/8
More suseptable to effects of gravity and gives rise to a great degree of vairability in blood flow within the lung

171
Q

which gs diffuses more rapidly and why

A

CO2: mose soluble - however overall rates of equilibrium between O2 and CO2 are similar because of the greater pressure gradient for O2

172
Q

how is the anatomy of the lung adapted to maximise gas exchange

A
  • large surface area
  • minimunm diffusion distance
  • thin cell membranes

(type 1 alveolar cell, capillary cell)

173
Q

factors to influence gas diffusion across alveoli

A
  • partial pressure gradient
  • gas solubility
  • available surface area
  • thickness of the membrane
  • distances
174
Q

Emphysema

A

destruction of alveoli reduces surface area for gas exchange

175
Q

Fibrotic lung disease

A

thickened alveolar membrane slows gas exchange. Loss of lung compliance may decrease alveolar ventilation

176
Q

Pulmonary oedema

A

fluid in interstitial space increases diffusion distance by seperating the alveoli from the capillary. Arterial PCO2 may be normal due to higher CO2 solubility in water - normally due to pulmonary hypertension

177
Q

Asthma

A

Increased airway resistance decreases airway ventilation - PO2 low in alveoli and blood

178
Q

Effect of fibrotic lung disease on ventilation and diffusion

A
  • Dec ventilation as resists stretch during inspiration
  • Dec diffusion as fibrous tissue resists diffusion
179
Q

What is the physical characteristics of emphysema

A

breakdown of alveolar membrane and loss of elastic tissue

180
Q

what can cause emphysema

A

smoking

181
Q

effect of emphysema on compliance, elasticity and overall effect on breathing

A
  • increased compliance so big change in lung volume for relatively small change in intrapleural pressure
  • Lost lots of elasticity due to breakdown of elastic fibres meaning elastic recoil during expiration less common - may need to invest muscular effort rather than it being passive

Inspiration easier, expiration incredibly difficult

182
Q

2 big things lost/negatives of emphysema

A

loss of elastic tissue and loss of surface area

183
Q

explain the effect of asthma on diffusion

A

affects airways rather than alveoli so little direct effect. However, can have big impact on ventilation, and therefore PAO2 (dec) and PACO2 (inc), which will subsequently limit diffusion

184
Q

Obstructive and restrictive lung disease definitions

A

Obstructive: obstruction of air flow, especailly on expiration
Restrictive: restriction of lung expansion, loss of compliance

185
Q

Describe some obstructive lung disorders

A
  • Asthma
  • Chronic Obstructive Pulmonary Disease (COPD) - chronic bronchitis, emphysema

Impact expiration greater?

186
Q

Give some restrictive lung disorders

A
  • Fibrosis (idiopathic, asbestosis)
  • Infant Respiratory DIstress Syndrome (insufficient surfactant production)
  • Oedema
  • Pneumothorax (get loss of lung expansion)
187
Q

restrictive lung disorders

A

restiction of lung expansion, loss of compliance
Therefore, greater change in intra-pleural pressure required to inc volume by same amount

188
Q

spirometry

A

technique commonly used to measure lung function - amount of air inspired or expired

189
Q

How can spirometry measuremnet s be classed

A
  • Static: only consideration made is the volume exhaled
  • Dynamic: time taken to exhale a certain volume is measured
190
Q

what can spirometry not measure

A

anything where residual volume is a component
(residual volume, total lung capacity, functional residual capacity)

191
Q

Explain FEV1/FVC

A

FEV1: forced expiratoy volume in 1 second - 4L (fit healthy yound adult male)
FVC: forced vital capacity - 5L

FEV1/FVC = 80% - should be able to expel 80% of air in first second

abdolute values decline with age, but ratio remains around 80%

192
Q

FEV1/FVC for obstructive lung diseases

A

~42%

193
Q

FEV1/FVC in restrictive lung diseases

A

~90%
Airflow is fine but total amount of aire that can be expired is restricted due to restriction in expansion (less air goes into lungs in the first place)

194
Q

Explain the effect of an obstrictive lung disorder (e.g. COPD) on FEV1 and FVC (and then ratio)

A
  • rate at which air is exhaled is much slower
  • Total expired volume (FVC) is also reduced (FRC may be inc)
  • Mayor effect is on airways and so FEV1 is reduced to a greater extent than FVC
  • Ratio also reduced

FEV1 = big dec
FVC = dec
Ration = dec

195
Q

Explain the effect of a restrictive lung disorder (e.g. pulmonary fibrosis) on FEV1 and FVC (and then ratio)

A
  • absolute rate of airflow is reduced (but only because total lung volume is reduced)
  • total volume is reduced due to limitations to lung expansion
  • ration remains constant or can inc as a large proportion of volume can be exhaled in first second

FEV1 = big dec
FVC = big dec
Ratio = unchanged or inc

196
Q

What is spirometery more effective in diagnosing

A

Obstructive diseases since people with restrictive lung diseases may still ahve a normal ration of FEV1 to FVC

197
Q

explain key point with pressure-volume relationship and inspiratory and expiraotry curves - and why this is the case (3 reasons)

A

Ir requires a greater change in pressure (from FRC) to reach a particular lung volume during inspiration, than to maintain that volume during expiration
This is:
1. overcome lung inertia during inspiration
2. overcome surface tension during inspiration
3. during expiration compression of the airways means more pressure is required for air to flow along them

198
Q

give effect of emphysema and fibrosis on pressure-volume curves

A

see pic 6

199
Q

Describe the pathophysioology of asthma

A

Over-reactive constriction of bronchial smooth muscle. Inc resistance, expiration phase most affected

200
Q

what do obstructive and restrictive lung diseases increase the work of

A

Obstructive: expiration
Restrictive: inspiration

201
Q

what is tthe ventilation-perfusion relationship

A

ventilation (air getting to alveol L/min) <—> Perfusion (local blood flow L/min)

ideally V=P

202
Q

what happens to both blood flow and ventilation across the height of the lung

A

decrease

203
Q

what is higher at the base of the lung (blood flow or ventilation)

A

Blood flow is higher than ventilation because arterial pressure exceeds alveolar pressure. This compresses the alveoli

204
Q

What is higher at the apex of the lung (blood flow or ventialtion)

A

ventialtion is higher and blood flow is low because arterial pressure ois less than alveolar pressure. This compresses the arterioles

205
Q

Where are ventilation and perfusion both greater for both cases (in terms of V+P mismatch)

A

at the base of the lung

see pic 7

206
Q

how does the ratio of ventilation to perfusion withing the lung change from base to apex and why

A

increases - due to effect of gravity

207
Q

where does the majority of V+P mistatch occur

A

in the apex - this is then auto-regulated to keep V:P ratio close to 1.0

208
Q

Describe autoregulation when blood flow>ventilation (at base of lung)

A

If ventilation decreases in a group of alveoli, PCO2 inc and Po2 dec. Blood flowing past those alveoli does not get oxygenated. Dilution of oxygenated blood from better ventilated areas = SHUNT
Response: Dec tissue PO2 around underventilated alveoli constricts their arterioles (pulmonary vasoconstriction) diverting blood to better-ventilated alveoli. Bronchial dialation also happens due to inc PCO2.
Constriction in response to hypoxia is particular to pulmonary vessels (systemic vessels dilate)

209
Q

response of pulmonary vessels to hypoxia

A

constriction

(systemic vessels dilate)

210
Q

autoregulation when ventilation > blood flow

A

alveolar dead space - occurs to small extent in apex of lung, and pathologically in pulmonary embolus

Wat happens: Alveolar PO2 inc, PCO2 dec

Response: Pulmonary vasodilation and to a lesser extent bronchial constriction

Effect: act to bring V:P ration close to 1 as possible

211
Q

Shunt effects

A
  • pulmonary vasoconstriction
  • Bronchial dilation
212
Q

alveolar dead space effects

A
  • Pulmonary vasodilation
  • Bronchial constriction
213
Q

shunt

A

passage of blood through areas of the lung that are poorly ventilated (V < P)

opposite of alveolar dead space

214
Q

alveolar dead space

A

alveoli that are ventilated but not perfused

215
Q

anatomical dead space

A

air in the conducting zone of the respiratory tract unable to participate in gas exchange as walls of airways in this region (nasal cavities, trachea, bronchi and upper bronchioles) are too thick

216
Q

Physiological Dead Space

A

Alveolar dead space + Anatomical dead space

217
Q

Respiratory sinus arrhythmia

A

a normal alteration in cardiac rhythm (HR) generated from the stimulation of the vagus nerve and changes in cardiac filling pressures during respiration

218
Q

why does Respiratory sinus arrhythmia (RSA) occur

A

If HR stayed constant then:
* during inspiration… inc Alveolar dead space
* During expiration… inc shunt

Ensures V:P ratio is close to 1 (matched)

219
Q

How does RSA occur

A

due to inc bagal activity (parasympathetic nerve innervating heart) during expiratory phase

220
Q

where in the lung is perfusion higher

A

base

221
Q

what makes the lungs more susceptible to the effects of gravity which gives rise to a great degree of variability in blood flow within the lung

A

low pulmonary arterial pressure (25/8)

222
Q

why does ventilation change acorss the lung

A

Changes in compliance

223
Q

function of respiratory sinus arrhythmia (RSU)

A

minimise ventilation:perfusion mismatch during breath cycle

224
Q

2 ways O2 travels in blood and proportion of each

A
  • in solution in plasma - 3ml O2 dissolve per litre plasma
  • bound to haemoglobin protein in red blood cells -200ml O2 per litre whole blood, 197ml of which is bound to haemoglobin in red blood cells
225
Q

volume O2 per litre whole blood

A

200ml

226
Q

How is CO2 transported in the blood

2 ways

A
  • 77% in solution in plasma
  • 23% stored within haemoglobin
227
Q

how much arterial O2 is extracted by peroipheral tissues at rest

A

25%

228
Q

percentage of oxygen in blood bound to RBC (haemoglobin)

A

More than 98%

229
Q

how many O2 molecules does each haemoglobin bind

A

4

230
Q

what is the major determinant to which haemoglobin binds (is saturated with) oxygen

A

partial pressure of oxygen - PO2

231
Q

what does alveolar ventilation determine… and what does that determine…

A

Alveolar ventilation –> Po2 of alveoli –> PO2 of plasma (O2 in solution) –> O2 carried in haemoglobin in RBC

232
Q

how does Hb bind to O2 at the alveoli

A

Takes O2 from plasma maintaining a partial pressure gradient that continues to suck O2 out of the alveoli, until Hb becomes saturated with O2

Hb + O2 <—> HbO2

233
Q

How long does it take for Hb to become saturated with O2 and how long is total contact time

A

O.25s after contact with alveoli
- total contact time of 0.75s

234
Q

O2-Hb dissociation curve

A

see pic 8

235
Q

what does Hb show in binding to O2

A

co-operative binding

236
Q

explain the saturation of Hb at different PO2’s

A
  • Hb almost fully saturated at the normal systemic arterial PO2 of 100 mmHg
  • Even at PO2 of 60mmHg though haemoglobin is still 90% saturated with O2. This permits a relatively normal uptake of oxygen by the blood even when alveolar PO2 is moderately reduced.

At normal venous PO2, there is still 75% reserve capacity

Big PO2 fall causes relatively small impact on O2 binding to Hb

237
Q

Anaemia

A

Any condition with res ults in a decrease in the oxygen carrying capacity of the blood (e.g. iron deficiency, haemorrhage, vit B12 deficiency)

238
Q

What happens to PO2 in anaemia

A

Nothing: PO2 normal despite total blood O2 content being low

239
Q

What will a low PO2 indicate

A

a low total blood O2 content

240
Q

Can RBC be fully saturated with O2 in anaemia

A

Yes: RBC still fully saturated as PO2 is normal

(only caveat is iron deficiency where number of O2 binding sites will be reduced, but those present will be saturated)

241
Q

what factors can change the affinity of Hb for O2

A
  • pH
  • PCO2
  • Temp
  • DPG
242
Q

if the Hb-O2 dissociation curve moves up/down x axis what change would be seen

A

little impact on O2 uploading at lungs

243
Q

Hb-O2 dissociation curve response to alkalosis

A

move left

better for retaining O2

244
Q

Hb-O2 dissociation curve response to acidosis

(e.g. excercisinng muscle)

A

Move to right

better for offloading O2

245
Q

Hb-O2 dissociation curve response to dec PCO2

A

move to left

better for retaining O2

246
Q

Hb-O2 dissociation curve response to inc PCO2

A

move to right

better for offloading O2

247
Q

Hb-O2 dissociation curve response to inc temp

A

move to right

better for offloading O2

248
Q

Hb-O2 dissociation curve response to dec in temp

A

move to left

better for retaining O2

249
Q

Hb-O2 dissociation curve response to no DPG

A

move to left

better for retaining O2

250
Q

Hb-O2 dissociation curve response to added DPG

A

move to right

better for offloading O2

251
Q

what causes the Hb-O2 dissociation curve tp move to the right

name it

A
  • Dec pH
  • inc PCO2
  • Inc body temp

Bohr effect —> aids O2 unloading at peripheral tissues due to dec affinity of Hb for O2 (e.g. when exercising)

252
Q

when would the Hb-O2 dissociation curve move to the left

A

to inc affinity of Hb for O2 (but harder for tissues to access O2) - why hypothermia is dangerous

253
Q

explain binding of 2,3-DPG and how if affects O2 affinity

A

The affinity of haemoglobin for oxygen is decreased by binding 2,3-diphosphoglycerate (2,3-DPG) synthesised by the erythrocytes. 2,3- DPG increases in situations associated with inadequate oxygen supply (heart or lung disease, living at high altitude) and helps maintain oxygen release in the tissues.

254
Q

Table of factors affecting arterial PO2

A

see pic 9

255
Q

explain effect of CO binding on haemoglobin

A

CO binds to haemoglobin to form carboxyhaemoglobin with an affinity 250 times greater than O2 - binds readily and dissociates very slowly so very problematic once dissolved in circulation

256
Q

effect of CO poisining

A

hypoxia, anaemia, nausea, headache, cherry red skin and mucous membranes. Respiration rate unaffected due to normal arterial PCO2. Potential brain damage and death.

257
Q

Treatment for CO poisining

A

provide 100% O2 to inc PaO2

258
Q

how is CO2 transported (include percentages)

long one ik but important

A

When CO2 molecules diffuse from the tissues into the blood, 7% remains dissolved in plasma and erythrocytes, 23% combines in the erythrocytes with deoxyhemoglobin to form carbamino compounds, and 70% combines in the erythrocytes with water to form carbonic acid, which then dissociates to yield bicarbonate and H+ ions. Most of the bicarbonate then moves out of the erythrocytes into the plasma in exchange for Cl- ions & the excess H+ ions bind to deoxyhemoglobin. The reverse occurs in the pulmonary capillaries and CO2 moves down its concentration gradient from blood to alveoli.

see pic 10

259
Q

what does alveolar PP equal

A

arteroid PP

260
Q

What does peripheral tissue PP equal

A

venous PP

261
Q

what is the sole determinant of arterial partial pressure of oxygen (PaO2) and in health is in equilibrium with alveolar partial pressure of oxygen (PAO2)

A

Oxygen in solution

262
Q

what is the main determinant of how much oxygen binds to haemoglobin (saturation)

A

PaO2

263
Q

what directly determines how much oxygen can bind to Hb and what else can influence it

A
  • PaO2
  • number of RBC
  • amount of Hb in each RBC

Influence:
* PaCO2
* Bondy temp
* Plasma pH
* levels of 2,3 DPG

264
Q

explain the action of carbonic anhydrase in CO2 transport

A

Once inside the RBC, the enzyme carbonic anhydrase catalyses the conversion of CO2 into carbonic acid (H2CO3). Carbonic acid is then hydrolysed into H+ ions and HCO3– (bicarbonate). The H+ ion is bound by haemoglobin which buffers the process.

265
Q

factors to favour CO2 unloading into the lungs

A

Same that inc O2 loading:
* High pH
* Low CO2
* Low temp
* No DPG

Haldane effect

maybe check???

266
Q

what is PaO2 not the same as

A

arterial O2 content

267
Q

what determines PaO2 (O2 in solution in the plasma)

A
  • O2 solubility
  • PO2 in the gaseous phase that is driving O2 in solution
268
Q

What is the PaO2 (oxygen tension)

A

100mmHg

269
Q

What is PP not the same as and why

A

concentration: conc varies on the form the molecule is in

270
Q

Do gases travel in the gaseous phase in plamsa

A

No (although bound to Hb), if they did they would cause air embolism

271
Q

how many ml of O2 bind to each gram of haemoglobin

A

1.34ml

272
Q

Types of Hb

A
  • 92% HbA
  • 8% mad up of HbA2, HbF, and glycosylated Hb
273
Q

Myoglobin

A

another O2 carrier molecule found exclusively in cardiac and skeletal muscle (only made of 1 poplypeptide chain)

274
Q

HbF

A

foetal haemoglobin

275
Q

Affinity of HbF and myoglobin for O2 compared to HbA

A

have higher affinity: necessary for extracting O2 from maternal/arterial blood

276
Q

why does myoglobin have a higher affinity for O2 that Hb

A

allows skeletal/cardio muscle to extract more O2 from blood

277
Q

difference between partial pressure and gas content

A

PP: amound dissolved in solution/plasma
Gas content: amount dissplved in plasma plus bound to Hb

278
Q

hypoxia definition

A

inadequate supply of O2 to tissues

279
Q

5 types of hypoxia

A
  1. Hypoxaemic Hypoxia: most common. Reduction in O2 diffusion at lungs either due to decreased PO2atmos or tissue pathology. (e.g. altitude)
  2. Anaemic Hypoxia: Reduction in O2 carrying capacity of blood due to anaemia (red blood cell loss/iron deficiency).
  3. Stagnant Hypoxia: Heart disease results in inefficient pumping of blood to lungs/around the body
  4. Histotoxic Hypoxia: poisoning prevents cells utilising oxygen delivered to them e.g. carbon monoxide/cyanide
  5. Metabolic Hypoxia: oxygen delivery to the tissues does not meet increased oxygen demand by cells.
280
Q

partial pressure

A

amount of oxygen in solution in plamsa

281
Q

what does higher affinity of HbF for O2 allow

A

them to extract O2 from (maternal) systemic circulation that would not otherwise have access too

Respiratory - Medicine 1 (1 decks)

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