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Physiology > respiratory physiology: ventilation and perfusion > Flashcards

respiratory physiology: ventilation and perfusion Flashcards

1
Q

what determines respiratory airflow?

A

the pressure difference between mouth and alveoli

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2
Q

what causes flow?

A

either an upstream rise (positive pressure breathing) or a downstream fall in pressure (negative pressure breathing)

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3
Q

what is positive pressure breathing?

A

generating a higher pressure in the mouth forcing air into the lungs
ventilation

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4
Q

what is negative pressure breathing?

A

generating a lower pressure in the lungs causing air to move into them from the mouth
normal breathing

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5
Q

Pip

A

intrapleural pressure/ intrathoracic pressure

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6
Q

Palv

A

alveolar pressure

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7
Q

Ptp

A

transpulmonary pressure

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8
Q

Patm

A

atmospheric pressure

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9
Q

Pip at rest

A

already negative due to counter recoil of chest wall/ alveoli and slight suction of excess fluid into lymphatic channels

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10
Q

what happens at inspiration?

A

Inspiratory muscles contract
Pip becomes more negative
increases difference between Palv and Pip which increases Ptp
alveolar volume increases so Palv decreases and increases the difference between Patm and Palv

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11
Q

What is Ptp

A

synoymous with alveolar wall distension

the larger Ptp is the greater the alveolar wall distension

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12
Q

What happens at expiration?

A

inspiratory muscles relax
Pip becomes less negative
decreases difference between Palv and Pip, decreasing Ptp
If Ptp is smaller the alveolar wall recoils due to elastin and collagen fibres
alveolar volume decreases causing Palv to increase and so increase the difference between Patm and Palv.

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13
Q

what is alveolar interdependence?

A

outer alveoli are affected by the change in intrapleural pressure
which affects the next alveoli and the next row until the inner depths of the lung

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14
Q

where is the visceral pleura?

A

membrane attached to lungs

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15
Q

where is the parietal pleura?

A

membrane attached to chest wall

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16
Q

what is between the visceral and parietal pleura?

A

intrapleural cavity/ space

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17
Q

what are the types of pneumothorax?

A

spontaneous
trauma
tension

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18
Q

what happens in a tension pneumothorax?

A

membrane breaks and there is infiltration of air into the thoracic cavity, it only comes in, it cannot leave. It compresses the heart and vessels causing cardiac tamponade

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19
Q

what happens in a pneumothorax?

A

the pleural seal breaks and air enters and gets trapped causing lung collapse

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20
Q

airway resistance

A

it is difficult to quantify in the conduction zone

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21
Q

what affects airway resistance?

A

branching, narrowing, dispensable, compressible airways

type of airflow

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22
Q

what are the different types of airflow through the airways?

A

laminar - linear
turbulent
transitional

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23
Q

what defines the changes in types of airflow?

A

reynold’s number

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24
Q

what is reynold’s number?

A

defines the airflow and is based on density of fluid, velocity, diameter of tube and viscosity of fluid

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25
Q

poiseuille’s law

A

resistance is directly proportional to viscosity of fluid and the length of tube and inversely proportional to the 4th power of radius (r^4) of tube

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26
Q

what conditions are associated with changes in tube radius?

A

asthma
bronchitis
croup

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27
Q

who are at greater risk of conditions affecting airway resistance/ radius?

A

children

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28
Q

why are children at greater risk of conditions affecting airway resistance/ radius?

A

smaller airways

higher resting respiratory rates

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29
Q

what can trigger contraction of smooth muscle in bronchi?

A 
PGD2 - prostaglandins
LTC4 - leukotrienes 
histamines
released during type 1 hypersensitivity 
TXA2
serotonin 
alpha adrenergic agonists 
ACh
low pp of CO2
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30
Q

what can cause an asthma attack

A

contraction of bronchial smooth muscle

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31
Q

how does bronchial muscle contraction occur?

A

trigger binds to muscarinic receptor (GPCR)
release calcium via IP3 into cell
forms calcium and calmodulin complex
activates myosin light chain kinase
myosin light chain (regulatory protein) around myosin head is phosphorylated by kinase and activates contraction

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32
Q

what mediates dephosphorylation of myosin?

A

myosin light chain phosphotase

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33
Q

what causes bronchiodilation

A

noradrenaline
adrenaline
B2 agonist - salbutamol

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34
Q

asthma

A

type 1 hypersensitivity
allergic or immediate hypersensitivity
develop IgE antibodies in response to harmless antigens

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35
Q

mechanism of asthma - type 1 hypersensitivity - initial allergen encounter

A

allergen is inhaled, ingested, injected or contact
antigen presenting cells pick up and present the allergen and adaptive immune response by B cells forming plasma cells to make IgE to allergen
IgE enter circulation and bind to mast cells in tissue

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36
Q

what happens in type 1 hypersensitivity on subsequent allergen encounter

A

allergen inhaled, ingested, injected or by contact
binds to IgE on mast cell
cross linking causes mast cell degranulation and release histamine, cytokines/ chemokines and leukotrienes (vasoreactive amines)

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37
Q

compliance

A 
high = good
low = bad
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38
Q

how is compliance measured

A

as volume per unit of pressure change
mLcmH2O-1)
value varies as lungs inflate

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39
Q

pressure volume pathway

A

is different taken during expiration and inspiration

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40
Q

what is average compliance of both lungs?

A

200ml air per 1cmH2O

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41
Q

why is there a difference in the pressure-volume pathway for inspiration and expiration?

A

differences in pressure applied to surfactant and recruitment of alveoli in inspiration and derecruitment in expiration

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42
Q

what is the pressure- volume pathway called?

A

hysteresis

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43
Q

what limits increase in pressure and volume in the lungs?

A

elastic limit of chest wall

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44
Q

what happens to compliance in Emphysema?

A

increases - left shift

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45
Q

what happens to compliance in fibrosis?

A

decreases - right shift

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46
Q

what does increased compliance suggest?

A

emphysema/ obstructive disease

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47
Q

what does decreased compliance suggest?

A

fibrosis/ restrictive disease

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48
Q

compliance curve

A

Ptp on x axis and Vol on y axis

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49
Q

emphysema

A 
destruction of alveolar walls - large air spaces that are no cleared of air on exhalation - air trapping . 
destruction of elastic fibres
reduced elastic recoil 
gas exchange decreases
O2 diffusion decreases
O2 levels in blood drop
50
Q

signs/ symptoms of emphysema

A

mild exercise causing breathlessness

barrel chest

51
Q

what causes emphysema?

A

consistent exposure to irritants - smoke, dust, chemical irritants
genetic predisposition due to alpha 1 antitrypsin deficiency

52
Q

what is emphysema part of ?

A

along with chronic bronchitis they are the 2 main causes of COPD

53
Q

what is chronic bronchitis?

A

inflammation of bronchial tubes and excessive mucus production causing coughing and SOB

54
Q

what are the diseases making up COPD?

A

chronic bronchitis

emphysema

55
Q

what is surfactant?

A

lipoprotein secreted by type 2 alveolar cells

part of the liquid film lining alveoli

56
Q

what does surfactant do?

A

lowers surface tension
increases compliance
improves work of breathing

57
Q

why is surfactant clinically important?

A

infant respiratory distress syndrome and acute respiratory distress syndrome

58
Q

what happens in IRDS?

A

surfactant not produced until 4 months gestation and not sufficiently until 7 months gestation or later

59
Q

what happens in ARDS?

A

reduction in surfactant production through injury to type 2 alveolar cells

60
Q

what is matched in the process of breathing and respiration?

A

ventilation and perfusion

61
Q

what is ventilation rate?

A

4-6L/min

62
Q

what is pulmonary blood flow?

A

4-6L/min

63
Q

ventilation/ perfusion

A

V/Q = 0.8-1.2

64
Q

what is the problem with ventilation/ perfusion matching?

A

there are regional differences so ventilation and perfusion need to be matched at the alveolar - capillary level

65
Q

ventilation distribution in healthy lungs

A

at start of inspiration, alveoli at the base of the lung are smaller and so have more capacity to expand - therefore ventilation to these areas is greater over the whole breathing cycle .

66
Q

perfusion distribution in healthy lungs

A

perfusion pressure falls if above level of heart and increases if below it . Blood flow increases steadily from apex to base .

67
Q

maximum PAP

A

pulmonary artery pressure

25/10mmHg

68
Q

ventilation-perfusion matching

A

greater ventilation at bottom of lung and greater perfusion at bottom of lung so they are generally well matched

69
Q

problems with V/Q matching

A

affects O2 and CO2 transfer

70
Q

pulmonary shunt

A

passage of deoxygenated blood from right side of heart to left without participation in gas exchange in the pulmonary capillaries. There is no ventilation and pulmonary arterial blood is not oxygenated

71
Q

Alveolar dead space

A

no perfusion
alveolar gas is the same as room air, containing not CO2
no blood flowing through their adjacent pulmonary capillaries

72
Q

severe ventilation/ perfusion abnormalities

A

pulmonary shunt

alveolar dead space

73
Q

less severe ventilation/ perfusion abnormalities

A

respiratory problems that produce a fall in FRC and compliance

74
Q

how does reduced FRC effect ventilation?

A

reduced volume causes reduced compliance due to increased airway resistance, airway collapse and lung collapse
causes apexes and mid-zones to have higher compliance and so ventilation becomes higher at the apex

75
Q

affect of falling FRC on V/Q matching

A

greater ventilation at apex of lung but greater perfusion remains at bottom of lung and so there is a mismatch - resulting in inadequate ventilation to oxygenate blood in base of lungs - hypoxia

76
Q

what is the importance of ventilation/ perfusion matching

A

efficient gas exchange requires them to be well matched

77
Q

what are the stages involved in carbon dioxide and oxygen transport?

A 
ventilation
external respiration
Gas transport
internal respiration
cellular respiration
78
Q

what happens in ventilation?

A

gas exchange between atmosphere and alveoli

79
Q

what happens in external respiration?

A

O2 and CO2 transfer between alveoli and blood

80
Q

what happens in gas transport?

A

O2 and CO2 carried in blood between alveoli and tissues

81
Q

what happens in internal respiration?

A

O2 and CO2 transfer between blood and tissues

82
Q

what happens in cellular respiration?

A

O2 utilisation and CO2 production by tissues

83
Q

how many divisions are there of the respiratory tree?

A

23

84
Q

which divisions are conduction airways?

A

1-16

tidal flow generated by respiratory muscles

85
Q

which divisions are respiratory exchange?

A

17-23

passive diffusion by partial pressure gradients

86
Q

passive diffusion

A

exchange of CO2 and O2 occurs by this, it is governed by dalton’s and Henry’s law

87
Q

what is Dalton’s law?

A

how gases move down their concentration gradient by diffusion

88
Q

what is Henry’s law?

A

how the solubility of a gas relates to its diffusion

89
Q

Dalton’s law

A

to do with partial pressure

90
Q

how is partial pressure calculated?

A

pressure exerted by a gas in a mixture

% in the mixture x ambient pressure (overall pressure) e.g. 21% O2 in air x atmospheric pressure (750mmHg) = 157mmHg§

91
Q

role of Dalton’s law in lungs

A

gases move from high partial pressure to lower partial pressure, so O2 moves down airways and CO2 moves up .
O2 moves from alveoli to blood and CO2 from blood to alveoli
determines the exchange of CO2 and O2 between atmosphere and lungs, lungs and blood and blood to tissue cells

92
Q

henry’s law

A

the quantity of a gas dissolved in liquid is proportional to partial pressure of the gas and solubility of the gas .
The higher the partial pressure and the higher the solubility of the gas the more gas will stay in solution
partial pressure in solution = partial pressure in gas phase

93
Q

what happens if you double partial pressure of a gas in gas phase?

A

double the amount of gas will be dissolved for a simple solution

94
Q

external respiration

A

diffusion of O2 and CO2 between air in alveoli and blood in pulmonary capillaries
converts deoxygenated blood to oxygenated
CO2 into alveoli and O2 into blood

95
Q

what type of process is external respiration?

A

passive/ independent

96
Q

another name for external respiration

A

perfusion

97
Q

internal respiration

A

exchange of O2 and CO2 between systemic capillaries and tissue cells
converts oxygenated to deoxygenated blood
CO2 into blood and O2 into cells

98
Q

what type of process is internal respiration?

A

passive/ independent

99
Q

what is the major determinant of oxygen in the blood?

A

partial pressure of O2

100
Q

how much oxygen is dissolved in plasma?

A

1.5% of inhaled O2

101
Q

oxygen carriage system

A

haemoglobin
deoxyhaemoglobin + oxygen –> oxyhaemoglobin
haemoglobin increases the total quantity of oxygen in blood greatly doesn’t change partial pressure of oxygen because partial pressure measures dissolved oxygen

102
Q

haemoglobin

A 
globin protein 
4 polypeptides 
2 alpha and 2 beta 
4 haem groups 
pigment 
one on each polypeptide
103
Q

haem group

A

porphyrin ring surrounding an iron ion (Fe 2+ - ferrous ion) linked to a globin chain

104
Q

binding to haemoglobin

A

each haem binds 1 molecule of oxygen - O2

binding is reversible

105
Q

process of binding

A

as the first oxygen binds the haemoglobin changes shape and becomes looser
making binding of the next oxygen easier
full saturation - binding of 4th oxygen is harder because there are fewer spaces available

106
Q

how much oxygen can 1g of haemoglobin hold?

A

1.34mL

107
Q

oxygen saturation curve

A

indicates that the saturation of haemoglobin depends on the partial pressure of oxygen
high pp = high saturation of haemoglobin
low pp = low saturation of haemoglobin

108
Q

what happens at the tissues?

A

as partial pressure of oxygen falls the saturation of haemoglobin falls because it unloads oxygen

109
Q

the bohr effect

A

in tissues that need more oxygen the local environment moves the curve to the right by helping unloading of oxygen

110
Q

how does the bohr effect work

A

as tissue metabolism increases lactic acid and CO2 concentration increase causing:
CO2 + H2O H2CO3 H+ + HCO3-
the H+ ions bind to haemoglobin and alter its structure decreasing its oxygen carrying capacity

111
Q

what happens in the lungs?

A

alveolar environment has high pp of oxygen and low of CO2 so is alkalotic and so moves the curve to the left and aids uptake of oxygen

112
Q

solubility of CO2 in plasma

A

25 times more soluble than O2 in plasma still has specialised transport systems

113
Q

what forms is CO2 carried in?

A

dissolved in plasma
bicarbonate
carbamino compounds
results in a CO2 content curve

114
Q

Proportions of different carbon dioxide carriage methods

A

HCO3-
carbamino
dissolved

115
Q

CO2 in the red cell

A

CO2 + H2O <> H2CO3 <> H+ +HCO3-
Bohr effect: H+ + Hb.O2 <> Hb.H+ + O2
CO2 + Hb.NH2 <> H+ + Hb.NH.COO- (carbamino)
The H+ needs buffering

116
Q

Haldance effect

A

works in tandem with the bohr effect to enhance CO2 transport

117
Q

Haldane effect in tissues

A

haemoglobin gives up O2
Affinity for CO2 increases (left shift)
greater CO2 carriage

118
Q

Haldane effect in lungs

A

haemoglobin gives up CO2
Affinity for CO2 decrease - right shift
Haemoglobin binds oxygen

119
Q

how the bohr and haldane effect work together

A 
bohr = O2 unloading/ loading enhanced by CO2 loading/ unloading 
Haldane = CO2 loading/ unloading enhanced by O2 unloading/ loading
120
Q

how are smooth muscles relaxed?

A

To relax myosin is dephosphorylated and Calcium and extruded from the cell into sarcoplasmic reticulum

121
Q

what does kinase do?

A

phosphorylates

122
Q

how do bronchodilators work?

A

bronchodilator causes release/ activation of protein kinase A
which phosphorylates the myosin light chain kinase which
deactivates it causing smooth muscle relaxation

Physiology (46 decks)

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