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Primary Physiology > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

Function of the respiratory system

A

Gas exchange
Immune defence
Metabolic
Filter for small emboli
Acid base

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2
Q

During quiet nasal breathing how much of total airway resistance comes from the upper airways?

A

2/3rds

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3
Q

Functions of the upper airways

A

Conduction of gas
Warm and humidify gas
Filter and immune
Vocalisation

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4
Q

Function of the larynx

A

Regulation of expiratory air flow - important for vocalisation, cough and control of end expiratory volume
Protection of lower airway
Vocalisation

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5
Q

Roughly how many times does an airway branch from trachea to alveoli

A

23

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6
Q

Adult tracheal length and diameter
Epithelium
Special function

A

11cm 18mm
Ciliates columnar with goblet cells
Mechano and chemical receptors to mediate cough

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7
Q

Angle of right main bronchi to trachea vs left

A

25o vs 45o

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8
Q

At what weibel level does cross sectional area rapidly increase?
Implication for air flow?

A

5-11 (small bronchi)
Lower flow velocity

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9
Q

Distinction between bronchi and bronchioles

A

No cartilage in bronchioles

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10
Q

Epithelial changes between large bronchi, small bronchi and bronchioles

A

Columnar epithelium of bronchi becomes cuboidal in respiratory bronchioles with gradual transition between the two over small bronchi and non-respiratory bronchioles. No goblet cells in bronchioles.

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11
Q

Diameter of bronchioles

A

<1mm

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12
Q

Character of respiratory bronchioles

A

Intermittent alveolar out pockets
Still has muscle layer and sphincters around alveoli

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13
Q

Size of alveoli
Total surface area

A

0.3mm diameter
50-100m2

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14
Q

Types of alveolar cell and function + adaptation

A

Type 1 - 80% of surface, gas exchange, very thin layer of cytoplasm, metabolically limited.
Type II - manufacture surfactant, high metabolic capacity
Type III - alveolar macrophages - proteolytic enzymes

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15
Q

How are alveoli connected?
Significance

A

Via respiratory bronchioles
Small (8-10micrometer holes) - pores of kohn - allows collateral ventilation

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16
Q

What composes the alveolar capillary membrane?

A

Alveolar epithelium
Interstitial tissue (fused alveolar and endothelial basement membranes)
Capillary endothelium

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17
Q

How are capillaries arranged around alveoli for gas and fluid exchange?

A

A close ‘thin’ connection for gas exhange
A thick side with interstitial space where fluid exchange can occur

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18
Q

Why are lymphatics important in the lungs

A

Accumulation of fluid would be bad and impair gas exchange

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19
Q

What are the lung volumes?

A

Inspiration reserve
Tidal
Expiratory reserve
Residual

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20
Q

What are the lung capacities

A

Total lung (all volumes)
Vital (inspiratory reserve, tidal and expiratory reserve)
Inspiratory (tidal and inspiratory reserve)
Functional residual (expiratory reserve and residual)

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21
Q

Total lung capacity of a male vs female
Where is most of the difference?

A

6000ml vs 4200ml
Inspiratory reserve volume 3300 vs 1900
Small differences in residual and expiratory reserve volume. Tidal volumes the same.

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22
Q

What determins vital capacity?

A

Body size
Strength of respiratory muscles
Chest and lung compliance

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23
Q

What is functional residual capacity?

A

The volume left in the lung at the end point of passive expiration where the tendency of the lung to collapse and the thoracic cage to expand are equal.

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24
Q

What causes reduced functional residual capacity

A

Supine or head down positioning
Age, posture
Pulmonary fibrosis, pulmonary oedema
Obesity, abdominal swelling
Thoracic wall distortion, reduced muscle tone

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25
Q

What increases functional residual capacity

A

Positive intrathoracic pressure
Emphysema
Asthma

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26
Q

How is functional residual capacity measured?

A

Helium dilution - fixed circuit spirometery with known concentration helium (insoluble), patient breaths mixing volume of gas mixture with FRC - amount helium is diluted gives FRC.

Body plethysmograph - patient in closed chamber and measure pressure and volume changes when subject makes inspiratory effort.

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27
Q

What gas law is needed to determine FRC by body plethysmograph

A

Boyles law

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28
Q

What needs to be introduced into the system during helium dilution measuring of FRC and why?

A

Oxygen to compensate for oxygen consumption.

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29
Q

What is closing capacity of the lungs

A

The volume at which airways collapse during expiration

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30
Q

What is the relationship between closing capacity and functional residual capacity

A

FRC always > CC under normal circumstance
If FRC decreases of CC increases in disease (e.g loss of elasticity) then airway closure may occur at end of normal expiration producing large areas of atelectasis on induction of anaesthesia.

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31
Q

Limitation of helium dilution

A

Non communicating air spaces

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32
Q

Mechanism of body plethysmograph for FRC measurement

A

Sit in sealed box with mouthpiece. At end normal expiration mouthpiece sealed but pt told to breath in. FRC volume thus expands. Pressure in box changes as fixed volume. Given pressure change volume change can be calculated by Boyles law.

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33
Q

Common dynamic lung volumes

A

Forced vital capacity - volume forcibly expired after maximal inspiration
FEV1 - volume forcibly expired in first second following vital capacity breath

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34
Q

Normal fev1:Fvc ratio

A

95%
Declining to 85% in elderly

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35
Q

What is ventilation

A

Process of fresh gas reaching the area of the lungs where fresh gas exchange takes place

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36
Q

What is dead space
Subdivisions

A

Areas of the lungs which are ventilated but that do not take part in gas exchange
Anatomical - conducting airways
Alveolar - areas ventilated but not perfused

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37
Q

How much anatomical dead space is there in an adult?

A

2ml/kg or 150ml on average

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38
Q

How can anatomical dead space be measured?

A

Taking a cast of the airways - historical

Fowler’s method

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39
Q

What is fowlers method for measuring anatomical dead space

A

patient takes a single vc breath of 100% o2 and exhales through a rapid nitrogen gas analyser
Nitrogen concentration is then plotted against expired volume
Three phases
1 - no nitrogen
2 - increasing nitrogen as alveolar air introduced
3 - plataeu
Dead space volume is the dividing line on phase 2 that gives an equal volume above the curve the right as below to the left (look at a picture)

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40
Q

What factors could influence anatomical dead space?

A

Changes in bronchial tone
Changes in position of head and neck
External breathing apparatus eg ett
Changes in tidal volume - low Tv causes laminar flow and decreasing dead space

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41
Q

What is the term for the proportion of a breath that reaches the alveoli (ie tidal volume - anatomical dead space)

A

Alveolar volume
Can be multiplied by respiratory rate to give alveolar ventilation

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42
Q

What equation is used to calculate physiological dead space?

A

Bohr equation

Vd/Vt = (PACO2 - PECO2)/PACO2
Or
Vd/Vt = PaCO2 - PECO2)/PaCO2

PA - alveolar co2 pressure
PE - expiratory gas co2 pressure
Pa - arterial co2 pressure - substituted in in clinical practice

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43
Q

What is physiological dead space

A

Anatomical dead space + alveolar dead space

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44
Q

Muscle actions of inspiration

A

Diaphragmatic flattening
External intercostals
Strap muscles (sternocleidomastoid, anterior serrati, scalenes)

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45
Q

Proportion of quiet ventilation provided by diaphragm alone?
Adaptation to constant use

A

75%
Lots of slow twitch so fatigue resistant

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46
Q

Main function of accessory muscles of inspiration during quiet inspiration? Forced inspiration?

A

Quiet - stabilisation of upper rib cage to prevent indrawing
Forced - elevation and expansion of rib cage.

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47
Q

Muscles used in quiet and forced expiration

A

Quiet - nil
Forced - abdominal muscles, internal intercostals

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48
Q

What determines resting volume of the lung at FRC

A

Pulmonary elasticity would cause collapse of lungs to smaller than FRC
Chest wall volume would be larger than FRC due to recoil
Thus combination of two opposing forces results in FRC volume as it is.

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49
Q

What couples the thoracic Cage (chest wall and diaphragm) to the components of the lung

A

The trans pulmonary pressure gradient

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50
Q

What is the interpleural pressure at end expiration?
How does it change on inspiration, normal and forced?

A

-0.3kpa
Normal inspiration -1kPa
Forced inspiration -4kPa

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51
Q

How can interpleural pressure be measure

A

Intrapleural catheter
Balloon cather in mid oesophagus

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52
Q

What is normal airway pressure during spontaneous respiration?

A

Atmospheric - the changes are all in the interpleural pressure

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53
Q

What causes lung expansion (sequence)

A

Contraction of respiratory muscles
Expansion of thoracic cage
Decreased interpleural pressure
Lung expansion to equalise

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54
Q

What is trans pulmonary pressure

A

The pressure difference between airway pressure and interpleural pressure

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55
Q

What is lung compliance

A

Lung compliance = change in volume / change in trans pulmonary pressure

Ie the amount of expansion achieved at a given transpulmonary pressure

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56
Q

Around normal FRC what is the relationship between interplumonary pressure and vital capacity

A

Roughly linear

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57
Q

What happens to compliance at high and low lung volumes

A

Reduced at high as elastic fibres are stretched to limit
Reduced at low because of airway collapse

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58
Q

Rough value for healthy lung and chest wall compliance at FRC

A

200ml / cm H2O

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59
Q

What reduces chest wall compliance

A

Diseases like ankalosing spondylitis making chest wall rigid

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60
Q

What is the overall respiratory system compliance

A

A combined chest wall and lung compliance
Overall compliance less than the individual ones

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61
Q

How can respiratory system compliance be measured?

A

Statically - apply a known distending pressure and wait to come to equilibrium (all movement to shift) and measure volume change

Dynamically - during spontaneous or mechanical ventilation plot change in vol with change in pressure constantly. Dynamic compliance derived from slope of curve produced

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62
Q

What would give a lower reading (less volume change for given pressure), static or dynamic compliance measurements?
Why?

A

Dynamic
Airflow may not have completely ceased on measurement (further volume increases could occur as air moves from less to more distendable regions)
A sustained pressure (as in static) causes relaxation of tissues due to their viscoelastic nature, thus gives a larger volume change
Inter pulmonary pressure will be lower than applied pressure due to resistance thus underestimate of compliance.

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63
Q

How does positioning change compliance?

A

Decreased compliance on moving from stood to supine

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64
Q

Effect of age on resp system compliance

A

Lower in infants and elderly

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65
Q

Diseases that can lower compliance

A

Ards
Pulmonary oedema
Ankylosing spondylitis
Pregnancy

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66
Q

What is the term for the phenomena of inspriatory and expiratory pressure volume curves not coinciding - what does it form?

A

Hysteresis
A pressure volume loop

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67
Q

What is the representation of the area of the pressure volume loop with hysteresis?

A

Lost energy as a result of viscous losses during stretching and recoil of the tissues and frictional losses of airway resistance

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68
Q

What way does a pressure volume loop run? Which limb is inspiration and expiration

A

Anti-clockwise
Rightmost limb (ascending) expiration

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69
Q

What is surfactant

A

A phospholipid secreted by type ii alveolar cells

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70
Q

Effects of surfactant

A

Reduces surface tension causing
- more even distribution of compliance
- stabilisation of small alveoli
- reduction of the energy lost in inspiration thus reduced hysteresis
- helps keep alveoli dry

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71
Q

How does decreased surface tension from surfactant act to increase and even compliance

A

Small alveoli disproportionately effected by surface tension with tendancey to collapse, thus surfactant reduces this and reduces overall tendency of alveoli to collapse

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72
Q

How does surfactant act to keep alveoli dry

A

Surface tension creates a negative pressure drawing fluid in, this is reduced by surfactant

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73
Q

What is the gravitational model of distribution of ventilation and perfusion in spontaneously breathing patient

A

Lung behaves as a volume of fluid with hydrostatic pressure greater at the base than apex.
This results in less negative interpleural pressure at base.
As a result apex is overdistended (on the flattening upper part of pressure volume curve with less compliance) and base is well distended with good compliance.
Thus on inspiration bases expand well delivering air to the well perfused (also due to gravity) lung bases.

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74
Q

What occurs to the gravitational model for distribution of ventilation and perfusion on ppv?

A

FRC is reduced thus bases now become at the flat part of the curve needing more pressure to ventilate and apexs enter good compliance zone - thus preferential distribution of air to poorly perfused apexes

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75
Q

What casts doubt on gravitational model of distribution of ventilation and perfusion

A

Heterogeneity in ventilation and perfusion seen in zero gravity
Differences in V/Q on same gravitational level can be bigger than the apex base gradient
Expected changes aren’t always seen in postural changes

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76
Q

What is the structural model of ventilation perfusion matching

A

That VQ remains matched due to changes in regional vascular resistance largely influenced by changes in lung volume (due to twinned system of vessels with airways). Still influenced by gravity but not dependant on it. Main determinant is local airway resistance allowing variation over the one gravitational level.

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77
Q

What influences gas flow through the airways

A

Transpulmonary pressure gradient
Airway resistance
Pattern of gas flow

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78
Q

What formulae determins gas flow through the airways

A

Hagen Poisuelle law

Flow = pi . pressure difference . r^4 / 8 . length . viscosity

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79
Q

What are the characteristics of laminar gas flow

A

Smooth
Circumferential layers sliding over one and other with fastest flow in centre

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80
Q

Characteristics of turbulent gas flow

A

Disordered
Eddies and whirls
Relatively flat velocity in overall direction of flow

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81
Q

How is likelihood of turbulent flow predicted?

A

Reynolds number

Re = 2 . radius . average velocity . gas density / viscosity of gas

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82
Q

What are the significant Reynolds number cut offs

A

<1000 likely laminar flow
>2000 likely turbulent flow

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83
Q

What impact does turbulent flow have on the pressure flow relationship of a gas in the airways compared to laminar

A

Increases the effective resistance
- pressure gradient proportional to velocity^2
- dependant on gas density not viscosity
- inversely proportional to radius^5

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84
Q

Where does turbulent flow commonly occur in the respiratory tree

A

Laryngeal opening
Large bronchi weibel 1-5

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85
Q

Normal sites of resistance to gas flow in airways

Why

A

Upper airways (nose)
Major bronchi

Cross sectional area increases exponentially with branching.

86
Q

How can airway resistance be accurately measured

A

Simultaneous recording of airflow and pressure gradient in more than and alveoli! Hard!

Could do interpleural pressure monitoring instead but some small variation in pressures due to resistances - especially in pulmonary oedema and fibrosis

87
Q

Clinical measures of airway resistance
Pitfall

A

FEV1
PEFR

Also rely on expiratory muscle activity, not just resistance.

88
Q

What factors influence airway resistance

A

Lung volume - higher volume decreases resistance
Bronchial smooth muscle tone
Histamine release
Properties of inspired gas - density and viscosity
Lower and upper airway obstructions
Anaesthesia

89
Q

Why do patients with high airway resistance purse lip breath?

A

Increases FRC (PEEP)

90
Q

What is the main determinant of bronchial smooth muscle tone
What causes reflex constriction

A

Parasympathetic control via the vagus
Stimulation of larynx, trachea or bronchi

91
Q

What are the effects of H1 and H2 receptor stimulation on airway resistance

A

H1 - bronchoconstriction
h2 - bronchodilator
Overall effect is bronchoconstriction

92
Q

What inhaled gas reduces airway resistance

A

Helium

93
Q

Causes of lower airway obstruction increasing resistance

A

Mucus plug
Tumour
Epithelial desquamation
Foreign body

94
Q

Quantitative Effect of anaesthesia on airway resistance
Why

A

Doubles it
Reduced FRC
Increased upper airways resistance

95
Q

Causes of decreased FRC under anaesthesia

A

Supine positioning - or worse, head down/pneumoperitoneum
Muscle relaxation (diaphragm rises), chest wall decreases in circumference
Atelectasis

96
Q

What elements of work are required for inspiration

A

Work to overcome elastic forces of the lung (compliance) stored as elastic energy
Work to overcome airway resistance during movement of air into the lungs
Work to overcome the viscosity of the lung and chest wall tissue (tissue resistive work)

97
Q

What are the fates of the energy used in the work of inspiration during normal respiration

A

Work to overcome in elastic energy returned as contraction on expiration
Work to overcome tissue and airway resistance lost as heat

98
Q

How can pathology of the lung effect work done

A

Need for expiratory work - asthma
Increased airway resistive work - copd
Increased compliance work - pulmonary fibrosis

99
Q

What is oxygen tension at sea level kPa
In mitochondira?

A

21.3 (0.21 x 101.3)
0.5

100
Q

What is the partial pressure of oxygen in the lower airways? Why different to atmosphere

A

Addition of saturated water vapour
0.21 x (101.3-6.3) = 0.21x95 = 20kPa

101
Q

Why is the partial pressure of oxygen in the alveoli different to that of the lower airways (after saturated water vapour has been accounted for)?
What does this depend on

A

Some oxygen is absorbed and co2 is secreted
Depends on:
Rate oxygen is introduced into alveoli (alveolar ventilation and FiO2)
Rate of removal by absorption into alveolar capillary blood
Rate of delivery of co2 by pulmonary capillary blood

102
Q

How do we calculate amount of oxygen absorbed in the alveoli?

A

Estimate using amount of carbon dioxide excreted (approximated as PACO2) x the respiratory quotient (as less CO2 excreted as O2 absorbed)

103
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - PaCO2/RQ

104
Q

Why is calculating PAO2 important

A

Determins pp gradient across alveolar membrane

105
Q

Rough normal oxygen consumption per min

A

250ml/min

106
Q

What would decreases alveolar oxygen concentration

A

Hypoventilation (at normal demand <4lpm)
Hyper metabolic states (eg sepsis)
Sodium bicarb infusion - increases co2
Decreased fiO2

107
Q

What determins alveolar co2 tension

A

Rate of delivery of co2
Rate of alveolar ventilation

108
Q

What is the effect of increasing alveolar ventilation on CO2 at low volumes compared to high

A

More marked reduction per unit increase below 6 litres then diminishing returns above this.

109
Q

What does the rate of gas transfer depend on

A

Properties of membrane - surface area, thickness
Properties of gas - solubility, molecular weight
Pressure gradient

110
Q

What is Ficks law of gas transfer

A

Rate of gas transfer = k x A x deltP / D
= (solubility / square root molecular weight) x area x pressure gradient / distance

111
Q

What Favours oxygen transfer over Co2 in the alveoli

A

Lower molecular weight
Greater partial pressure gradient

112
Q

What favours Co2 over o2 in diffusion across alveoli?

A

Higher solubility (blood gas coefficient) - 24x that of oxygen

113
Q

How far does a red blood cell get past an alveoli before it is fully o2 saturated in health and normality?
What is the effect on o2 and co2 of making the diffusion gradient harder?

A

Around half
Harder gradient (e.g. fibrosis, oedema increasing depth or decreased area) effect o2 much more than co2

114
Q

What proportion of oxygen is transported in blood by what means

A

Hb 97%
Dissolved 3%

115
Q

What determins how much oxygen is dissolved in blood?
How much oxygen is typically dissolved in blood

A

Linear relationship with PAO2
0.023 ml/kPa/100ml
Thus at PAO2 of 13 = 0.3ml/100ml dissolved O2

116
Q

How much oxygen would be dissolved in blood if FiO2 was 100% and pCO2 5 and RQ 0.8

A

PAO2 = 95 - 5/0.8 = approx 90
Dissolved O2 = 90 x 0.023 = 2.07ml/100ml blood

117
Q

What is the structure of haemoglobin
Iron state?

A

4 subunits each with ferrous (Fe2+) atom

118
Q

Normal adult Hb proportions

A

98% HBA1 - 2 alpha 2 beta
2% HBA2 - 2 alpha 2 delta

119
Q

Fetal Hb chains
Other difference to adult chains

A

2 alpha 2 gamma
Lower affinity for binding 23DPG increasing affinity for oxygen

120
Q

How does 23 DPG work?

A

Binds to deoxygenated haemoglobin significantly reducing affinity for o2 facilitating unloading of oxygen in tissues with low oxygen tensions

121
Q

When is fetal hb replaced by adult hb

A

Beta chain production starts after birth replacing gamma chains over first year of life
Majority is HbA by 6 months

122
Q

What are key capharacteristics of oxygen binding to Hb

A

Expends primerily in local oxygen tension PaO2
Is effected.p by local mediators (co2, 2.3.dpg, ph temp)
Produces an a,listeria changing in hb to relaxed form creating cooperative binding (as one binds easier for more to bind)

123
Q

What is the effect of co2 binding to hb called, how does it work

A

Haldane effect
Deoxygenation of hb increases affinity of proton binding sites enhancing ability to transport co2 from tissues to lungs

124
Q

What is the effect of a left or right shift on the oxyhaemoglobin dissociation curve

A

Left shift, higher saturation at given tension, more likely to retain o2 (higher affinity)
Right shift reverse

125
Q

Causes of left shift on oxyhaemoglobin dissociation curve

A

Hypothermia
Alkalosis
Decrease CO2
Decreased 2.3.DPG
Presence of HbF

126
Q

What cause right shift on oxyhaemoglobin dissociation curve

A

Acidosis
Raised co2
Raised temp
Raised 23DPG

127
Q

What causes the sigmoid shape of the oxyhaemoglobin dissociation curve
What value can be used to characterise it?

A

The allosteric modulation of hb by o2 causing cooperative binding
The p50 - oxygen tension at which 50% hb is saturated

128
Q

What is the name for the effect of the shift in the oxyhaemoglobin dissociation curve caused by co2 entering or leaving blood
How does it work

A

Bohr effect
Co2 enters red cell combines with water and dissociated to h and bicarb
Increased h then shifts ohd curve to right releasing o2
Bicarb moves out of RBC and Cl in
Process reversed at lungs

129
Q

How much o2 can be carried on Hb

A

1.34 ml per g Hb (practically, theoretically 1.39)
= SaO2 x 1.34 x Hb x 0.01
So with some easy typical values
= 100 x 1.34 x 15 x 0.01 = 20.4ml/100ml

130
Q

What is the theoretical oxygen carrying capacity of Hb? Why is it higher than the actual?

A

1.39ml/gHb
Higher than actual of 1.34 because of abnormal Hb like COHb

131
Q

What is the formulae for the total oxygen carrying capacity of blood

A

CaO2 = (SaO2 x 0.01 x Hb[g/dl] x 1.34) + (0.023 x PAO2)

132
Q

What is oxygen delivery
How is it calculated
Rough values

A

The amount of o2 delivered to the peripheral tissues per minute
CaO2 x Cardiac output
20ml/100ml x 5L/min
1L oxygen delivered per minute

133
Q

What is oxygen uptake?
Formula
Typical values

A

Amount of oxygen taken up by tissues per minute
VO2 = Delivery of oxygen (CaO2 x CO) - return of oxygen (CvO2 x CO)
= 1000 - 750
= 250ml/min

134
Q

How does the body increase do2
What occurs in extreme demand?

A

Increase Co as hb and SpO2 pretty fixed
Cardiac output can’t increase enough, tissue demand exceeds body’s capacity to deliver, SvO2 falls, extraction ratio increases and tissue hypoxia occurs.

135
Q

What is the difference between venous and arterial co2 in blood
Pressure and Volume

A

About 0.7kpa
Around 4ml/100ml

136
Q

Out of the 4ml of CO2 added to arterial blood through the capillary bed where does it distribute?

A

2.8ml 70% enters erythrocytes forming carbonic acid, this dissociates then is buffered by deoxHb with tissue exchange of bicarb for Cl ions
0.9 ml 22% as carbamino compound - mainly with Hb
0.3ml 8% in solution

137
Q

Why is the hct of venous blood greater than arterial

A

Shift of Cl ions in causes increase in erythrocyte volume

138
Q

What are the body stores of oxygen (volume and location)
How long will these last before low enough that severe hypoxia occurs

A

1.5L
50% in Hb
30% in lungs
20% in myoglobin

3-4mins

139
Q

If normal body oxygen stores are around 1.5L how much are they increased to with preoxygenation

A

4.25L by increasing lung storage

140
Q

Rough body store of co2?
Effect of apnea on this?

A

Around 120L
Apnea increases it by about 1kPa in first minute then about 0.4kPa a minute after as passive diffusion up the apneic airways occurs

141
Q

What are the characteristics of the pulmonary circulation in terms of pressure and resistance

A

Low pressure - about 20% of systemic
Low resistance

142
Q

Rough time frame that blood takes to pass through pulmonary capilaries

A

0.5-1s

143
Q

What are the effects of alpha and beta adrenergic stimulation and vagal stimulation on pulmonary circulation?

A

Alpha - constricts
Beta - dilates
Vagal - dilates

144
Q

What is the supply of blood to the supporting tissue of the lungs (connective tissue, septa, bronchi)? Where does it drain?

A

Bronchial arteries from the thoracic aorta
Drains into the pulmonary veins causing anatomical shunt

145
Q

Why is left ventricular output greater than the right

A

1-2% of blood is supplied by the bronchial arteries draining directly back into the pulmonary vein and thus left ventricle bypassing the right.

146
Q

Normal pulmonary artery, capillary and vein pressures?

A

Artery 25/8mmHg MAP 15
Capillaries 10mmHg
Vein 4 mmHg

147
Q

What happens to right ventricular and pulmonary artery pressures on increased cardiac output?

A

Not much change due tot he distensibility of the pulmonary vasculature

148
Q

Factors that influence pulmonary vascular resistance?

A

Autonomic innervation
Nitric oxide
Prostacyclin
Endothilins
Vascular transmural pressure
Lung volume
Lung disease
Hypoxia vasoconstriction.

149
Q

What is the role of autonomic innervation on pulmonary vascular resistance

A

Pretty minimal, no tone at rest, sympathetic tone causes some vasoconstriction when triggered

150
Q

What is the origin of nitric oxide in the lungs? How does it act?

A

Derived from l-arginine in endothelium
Increases intracellular concentration of cGMP causing vasodilation

151
Q

What is the effect on lung vasculature of the endothelium dervived determinants of PVR

A

NO dilates
Prostacyclin dilates
Endothelinis constrict

152
Q

Origins of prostacyclin and endothelins

A

Prostacyclin - arachidonate
Endothelins - peptide

153
Q

What is the impact of vascular transmural pressure on PVR? Why?
Relevance to anaesthetics

A

Thin collapsible vessel walls
Higher airway pressures cause collapse and increase PVR
Thus PPV under anaesthesia can cause increased PVR

154
Q

How does change in lung volume effect PVR

A

Effects vessel calaber
As lung increases in volume vessels stretch and elongate becoming narrower

155
Q

How does lung diseases alter PVR

A

Acute and chronic lung disease can increase pvr

156
Q

How does pulmonary hypoxia alter pvr

A

Hypoxia vasoconstriction causing increase pvr

157
Q

What acts to initiate hypoxia pulmonary vasoconstriction

A

Small pulmonary arteries
To a lesser extent capillary bed and venous system

158
Q

Function of hypoxic pulmonary vasoconstriction

A

Improves vq matching diverting blood away from poorly oxygenated areas
Can be generalised however and can cause significant increases in PVR eg in foetus or at high altitude

159
Q

What drugs potentiate hypoxic pulmonary vasoconstriction

A

Cox inhibitors
Propranolol
Almitrine

160
Q

What drugs attenuate hypoxic pulmonary vasoconstriction

A

Volatile anaesthetics
Nitrates
Nitroprusside
Calcium channel blockers
Bronchodilators

161
Q

What factors can result in pulmonary hypertension?

A

Intracardiac shunt (asd/vsd)
Increased lvedp (mitral stenosis, constrictive pericarditis)
Obilteration - pulmonary fibrosis
Obstruction - emboli
Vasoconstriction - sleep apnea, high altitude
Idiopathic

162
Q

What are the functional zones of the lungs in the gravitational model for ventilation perfusion
Issues with model

A

Zone 1 (apex) - alveolar pressure created than arteriolar pressure and venous pressure, both arteriole and vein collapse obstructing blood flow. This part of the lung becomes alveolar dead space.
IN PRACTICE ZONE 1 DOES NOT EXIST, ARTERIOLAR PRESSURE ALWAYS MORE THAN ALVEOLAR - except in cases of decreased blood pressure such as hypovolaemia or increased alveolar pressure such as PPV or PEEP.

Zone 2 - alveolar pressure greater than venous pressure but less than arterial pressure, blood flow is partially obstructed - the collapsed veins open in systole or if pulmonary artery pressure increases

Zone 3 - alveolar pressure less than venous and arterial pressure. Blood vessels patent. Blood flow increases by recruitment of closed vessels and dilation of those already open. Causes decreased PVR

163
Q

Where does zone three of VQ lung gravity model extend?

A

To about 10cm above heart

164
Q

What are the terms for the zone 2 effect in the VQ of the lungs

A

Starling resistor
Waterfall effect

165
Q

Looking at the zone theory of VQ matching in the lungs what happens on lying supine? What about exercise

A

All zones become like zone 3 pattern

166
Q

What is a physiological shunt

A

When blood passes an inadequately ventilated alveoli with too greater perfusion for gas exchange to occur
V/Q <1

167
Q

What is alveolar dead space

A

Where full alveoli do not receive perfusion
V/Q >1

168
Q

What casts doubt on the gravitational model of VQ matching

A

There is significant heterogeneity over one gravitational plane of the lung
The VQ ratio at the apex is around 3.3 and base 0.6 so isn’t perfect by any stretch

169
Q

What is the normal A-a gradient
What causes it

A

0.5 - 1 kPa
Sum of the pO2 gradients across alvolar capillary membrane
Effect of shunted blood

170
Q

What would cause an increase in A-a gradient

A

Increase in diffusion barrier
Increase in shunt

171
Q

Causes of physiological shunt

A

Venous blood entirely bypasses lung (eg thebesian veins, bronchial veins, cardiac shunts)
Blood passes through areas that are not adaquetly ventilated V/Q <1 (eg pneumonia)
Blood passes through areas that are not ventilated at all V/Q 0

172
Q

What proportion of physiologically shunted blood becomes an issue?

A

<10% not clinically significant
>30% poor survival

173
Q

What is the shunt equation

A

Shunt flow/total flow = reduction in oxygen due to shunt/total oxygen added by lungs

174
Q

What are the different levels of ventilatory control?

A

Medulla - inspiratory and expiratory centres
Pontine - pneumotaxic and apneustic centres
Cortical and limbic areas

175
Q

How do the medullary centres of respiration control interact?

A

Reciprocal innervation
As activity increases in one centre inhibitory signals are relayed to the other.

176
Q

Where is the inspiratory centre of the medulla?
Function

A

Dorsal medullary reticular formation
Source of basic ventilatory rhythm
During inspiration increased activity to muscles of inspiration.
During expiration increasing amounts of activity increase inhibition of expiratory centre until inspiration begins.

177
Q

Where is the expiratory centre?
Function

A

In the ventral medullary reticular formation
During inspiration gradually increasing activity arises from the expiratory pool inhibiting the inspiratory pool until expiration begins.

178
Q

What is the location and function of the pontine centres of respiration

A

Pneumotaxic centre in upper pond fine tunes ventilatory rate and tidal volume to minimise work - it limit the inspiratory centre limiting tidal volume and causing variation in respiratory rate.
The apneustic centre in the lower pons prolongs the inspiratory phase by stimulating the inspiratory centre
The area above this centre causes apneustic breathing (slow breath in, rapid out)

179
Q

What would happen to respiration if the pons was destroyed.

A

Medulla centres would keep on going - breathing would continue just without the fine tuning.

180
Q

What reflexes are involved in ventilation control

A

Chemoreceptors
Chemical and pressure receptors in airways
Stretch receptors in lungs
Golgi organs and muscle spindles

181
Q

Where are chemoreceptors located

A

Central - bilaterally beneath ventral surface of medulla
Peripheral - carotid bodies bilaterally at bifurcation of common carotid and aortic bodies along arch of aorta.

182
Q

What is the key stimuli at chemoreceptors?

A

Central - hydrogen ion concentration
Peripheral - oxygen delivery (concentration/flow)

183
Q

What receptors sense change in carbon dioxide/hydrogen ion concentration (speed and magnitude of response)

A

Much greater magnitude from central chemoreceptors however, peripheral stimulation occurs five times more rapidly so initiates response

184
Q

Neuronal supply to peripheral chemoreceptors

A

Carotid - Herings nerve to glossophayngeal
Aortic - vagal

185
Q

What is the effect of simulation of the chemical and irritant receptors of the upper airways and trachea?

A

Laryngeal closure
Apnea
Hyperpnoea
Bronchoconstriction

186
Q

What are the location function of the pressure receptors of the airways?

A

Located in smooth muscle of all airways and help control depth of respiration.

187
Q

What are the J receptors and what is their role in respiratory control

A

Located in alveolar walls
Triggered by engorgement of pulmonary capillaries eg heart failure
Stimulation results in rapid shallow breathing or apnoea

188
Q

What and where are the pulmonary stretch receptors
Eponymous name of reflex evoked? Strong or weak in humans?

A

In airway smooth muscle
Hering-Breuer reflex
Inhibit inspiration on response to lung distension - in humans quite significant though, can breath spontaneously with CPAP of 40 and probably only activates as protective mechanism with tidal volumes >1.5L

189
Q

Where are golgi tendon organs located in the control of ventilation
What do they do

A

Intercostal muscles
Inhibitory to the inspiration centres on distension

190
Q

What is the effect of muscle spindle in diaphragm and inspiratory muscles on control of ventilation?

A

Activate when particularly intense ventilation required eg airway obstruction.
May be responsible for sense of dysponea

191
Q

What is the response of the lungs to co2 levels?

A

No effect when below normal. When >4 increasing PaCO2 increases alveolar ventilation in a linear manner - around 1L/min extra for every 0.1kPa increase in PaCO2
Flattens at very high levels of co2 due to central depression, narcosis and respiratory depression.

192
Q

What factors would alter the curve of PaCO2 and alveolar ventilation? How?

A

Sleep, barbiturates, and morphine - reduces gradient of line and displaces to right (lower alveolar ventilation at a given PaCO2)
Work of breathing - high work of breathing also causes reduced response to CO2
Oxygen levels - concomitant decrease in pO2 causes marked shift to left (increased response to raising CO2)
Effected by age, genetics and race.

193
Q

How does raised CO2 cause increase alveolar ventilation?

A

Increased H+ centrally
Small response to increased H+ and PaCO2 peripherally

194
Q

How do sleep, very high Co2 and sedative medications cause decreased response to PaCO2?

A

Decreased in the central sensitivity of respiratory centers

195
Q

How does increased work of breathing decrease sensitivity to CO2

A

Reduced peripheral response to central drive

196
Q

What is the response to prolonged raised CO2 (timeframes)
Why

A

Maximal response over first few hours
Decreases to about 20% of maximum after 48hrs

Renal adjustment of H by reabsorption of bicarb
Bicarb diffusing centrally to normalise central pH

197
Q

What is the effect of varying PaO2 on alveolar ventilation

A

Very little until PaO2 <8kPa then exponential increase in ventilation

198
Q

How is the ventilatory response to hypoxia controlled

A

Virtually all peripherally
Hypoxia depresses central function which results in Cheyne Stokes breathing

199
Q

What is the effect of varied PaCO2 on ventilatory response to changes in PaO2

A

Marked increase in sensitivity and exaggerated effect

200
Q

What is the effect of voletile anaesthetics on hypoxic ventilatory drive

A

Suppresses it

201
Q

What is the effect of altitude on ventilatory drive

A

Hypoxia drives tachypnea but this is blunted by lower than normal CO2 production
On acclimatisation CO2 production increases and ventilatory response to the hypoxia increases

202
Q

Mechanisms of airway in immune defence

A

Filtration in nasal passage
Sneeze and cough reflex
Mucociliary clearance
T and B lymphocytes
Macrophages and neutrophils

203
Q

Effect of anaesthesia on lung immune defence

A

Bypasses filtration of nose
Paralyses cilia in mucociliary escalator

204
Q

Immunoglobulin types secreted in the airways?

A

IgA - promotes clearance of microorganisms
IgG - opsinoisation of microorganisms

205
Q

What is a nine respiratory function of the lungs that arise from all blood passing through its small capillary bed?
How else is it adapted to this function

A

Filtration - catches small clots for fibrinolysis
Rich in endogenous heparin

206
Q

What metabolic processes occur in the lungs?

A

Extracellular metabolism of bradykinins and adenine nucleotides
Intracellular metabolism of NA, prostaglandins, ANP
Activation of angiotensin 1
Sythesis of somatostatin, substance P, nitric oxide, prostacyclin
Release of prostaglandins, histamine, kallikreins, platelet activation factor
Surfactant production
Uptake and metabolism of anaesthetic agents

207
Q

What is the proposed mechanism of lung injury in ARDS

A

Abnormal actions of oxidative radicles and elastases on lung tissue

208
Q

What is kPa pressure at approx 5500m
What would PIO2 be at this level?
What can PAO2 fall too, how does the body adapt to this

A

50 (half of sea level)
50-6.3 x 0.21 = 9.2kPa (compared to 20 at sea level)
PAO2 can fall to 2.6kPa (9.2-(5.3/0.8))
Adapts with marked hyperventilation which lowers pCO2 and thus raises PAO2

209
Q

What is the pattern in response of alveolar ventilation to high altitude

A

Initial rapid increase in resp rate (due to hypoxic stimulation of chemoreceptors, then inhibition due to reduced Co2 and alkalosis) then a slow steady rise of over a number of days (renal elimination of bicarb, bicarb shifts out of CSF densinsitising chemoreceptors)

210
Q

What are the main changes of acclimatisation?

A

Hyperventilation
Polycythaemia
Increased 23DPG with right shift of oxyhaemoglobin curve
Increased capillary density
Increased mitochondrial density
Increased pulmonary artery pressure (due to hypoxic vasoconstriction)
Increased ventilatory capacity
More even distribution of perfusion (as less pressure gradient and higher PA pressures)

211
Q

What pathological processes can occur at high altitude

A

HAPE and HACE
right ventricular hypertrophy
Muscle atrophy and catabolism
Anti diuresis and oedema
Increased thyroid activity
Sleep disturbance
Impaired nervous system performance

Primary Physiology (15 decks)

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