Lecture 4- Clinical application in ventilation and lung mechanics Flashcards
1
Q
conducting portion of the resp tract
A
nasal cavity pharynx larynx trachea primary bronchi sedcondary bronchi bronchioles terminal bronchioles
2
Q
resp portion
A
resp bronchioles
alveolar ducts
alveoli
3
Q
alveoli made up of
A
type 1 pneumocytes- gas exchange
type 2 pneumocytes- surfactant
4
Q
QUIET INSPIRATION
A
• Inspiratory muscles contract Chest wall expands, taking lung with it (need pleural seal)
– To expand chest wall need functioning nerves, muscles, bones
– To expand lungs need to overcome
Elastic properties of alveolar walls
Surface tension of alveolar fluid
• Then air flows in:
• Overcoming airways resistance
5
Q
QUIET EXPIRATION
A
• Passive process:
– Needs elastic recoil of Lungs
– Need to overcome airways resistance
6
Q
compliance is a measure of
A
- Compliance is a measure of distensibility- change in volume relative to change in pressure
7
Q
e.g. low compliance in
A
brand new balloon
8
Q
e.g. high compliance in
A
older balloon (easier to blow up)
9
Q
elastance is a measure of
A
elastic recoil
the tendency of something that has been distended to return to its original size
10
Q
o In tissue with high compliance
A
easier to stretch, elastic recoil is less
11
Q
o In tissues with low compliance
A
- elastic recoil is high (tendency to return to original size)
12
Q
Lung Elasticity represents
A
mechanical properties of the lungs to be expanded (distended) by pressures surrounding or inflating the lungs, and to collapse
as soon as pressures disappear (lung recoil and distensibility)
13
Q
E.g. the higher the compliance (the more distensible)
A
the worse the elastic recoil – e.g. go back to original shape
14
Q
E.g. the lower the compliance (less distensible- harder to inflate)
A
the better the elastic recoil e.g. lung fibrosis
15
Q
ventilation also dependent on airways resistance which depends on
A
o Surface tension within airways o Diameter airways Mucous in airways Pulmonary pressure gradients Radial traction
16
Q
lung compliance is inverselys related to
A
connective tiussue surroundig alveoli- elastoc fibres inc collagen and other matrix elemets within the lug parenchyma
17
Q
the more elastic fibres in the connective tissue surrounding the alveoli
A
the lower the compliance- harder to inflate lungs
18
Q
The greater the alveolar surface tension, the
A
lower the lung compliance. (inversely related)
o Surfactant decreases surface tension, therefore increasing compliance
19
Q
lung elastic recoil is directly related to the amount of
A
connective tissue surrounding alveoli - elastic fibres including elastin & collagen and other matrix elements within the lung parenchyma (the more connective tissue the higher the elastic recoil)
20
Q
lung elastic recoil is ALSO directly related to
A
alveolar fluid surface tension
o If we have a condition where there is little surfactant- high alveolar surface tension- low compliance - lung elastic recoil will be increased
21
Q
lung elastic recoil is inversely related to
A
lung compliance
0 the higher the compliance, the less elastic recoil
22
Q
small bronchus have
A
small islands of cartilage and glands in submucosa
23
Q
bronchioles have
A
no caritlage or no glands
24
Q
how do bronchioles stay open on expiration if they have no cartilage
A
radial traction
25
radial traction
outward tugging action of the surrounding alveolar wall on bronchioles- tether them open
- Prevents collapse of bronchioles on expiration
26
Why is airway obstruction worse in expiration than inspiration?
- Insp- negative pressure in the pleural space during insp helps to keep lower airways open
- Ex- positive intrapulmonary pressure during ex exacerbates narrowing of intrathoracic airways
During inspiration the volume of the lungs increases so the pressure in the lungs decreases (more negative).
During expiration, the volume of the lungs decreases meaning the intrapulmonary pressure goes up, pushing on the bronchioles which don’t have cartilage- must have radial traction from the alveolar network.
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ATELECTASIS
– lung collapse – several causes
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INTERSTITIAL LUNG DISEASE
Lung expansion difficult secondary to stiff lungs from increased collagen in
alveolar walls – decreased compliance
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HYPOVENTILATION
- Inability to expand chest- many causes
30
PNEUMOTHORAX
- Air in the pleural space with loss of pleural seal
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OBSTRUCTIVE LUNG DISEASE (COPD&ASTHMA)-
↑airways resistance and, in emphysema decreased elastance secondary to loss elastin – compliance actually increased
32
RESPIRATORY DISTRESS SYNDROME NEW BORN -
↓ surfactant leads to increased surface tension and decreased compliance
33
in simple terms atelectasis is the inadequate expansion of air space- alveolar collaps and has 3 causes
- Impaired pulmonary surfactant production or function collapse- alveoli collapse secondary to surface tension
- Compression collapse: due to:
o Air in pleural cavity (pneumothorax)
Air
Liquid
Tumour
o Fluid in the pleura
- Resorption collapse: due to obstruction
o Airway obstructed; air downstream of blockage slowly absorbed into blood stream= empty alveolar = collapse
34
Compression collapse: due to:
```
o Air in pleural cavity (pneumothorax)
Air
Liquid
Tumour
o Fluid in the pleura
```
35
- Resorption collapse: due to obstruction
o Airway obstructed; air downstream of blockage slowly absorbed into blood stream= empty alveolar = collapse
36
How does atelectasis it cause impaired respiratory function?
- Alveoli not ventilated
o So cant participate in gas exchange- impaired oxygenation and CO2 elimination
- Also, collapsed alveoli more susceptible to lung infection inc. pneumonia
37
resportion collapse
Resorption collapse
| - Due to obstruction of large airway e.g. lung cancer, mucous plugs
38
interstitial lung disease
200 different types of disease
- Thickening of pulmonary interstitium (not the alveoli)
o Sometimes reversible= sometimes not
- if not reversible, or if reversible but cause not diagnosed, almost always results in lung fibrosis (increased collagen due to inflammation)
- Early detected / treatment key to preventing irreversible progression
39
thickening of the pulmonary interstitium in ILD is caused by
too many elastic fibres
| - alveoli have reduced compliance and wont inflate
40
histology in ILD
shows thickening of intersitium between alveoli
41
ILD also affects
gas exchange
i.e. not just air movement in an airway- also diffusion problem.
In interstitial lung disease (diffuse lung fibrosis)
• alveolar capillary membrane is thickened
• Increases diffusion distance for O2 and CO2 (Diffusion defect)
• Impairs gas exchange (more next week) Normal lung
42
Features of ILD
- Lung compliance reduced
o Lungs are stiff and hard to expand
- Elastic recoil of lungs is increase, the resting lung volume is smaller than normal, but rate of airflow not impaired
- Restrictive type of ventilatory defect on spirometry
43
Clinical symptoms of ILD
- Dry cough
- Dyspnoea (short of breath) on exertion progressing to at rest
- Fatigue
- Typically gradual, insidious progression Sx
44
Signs of ILD
- Decreased lung excursion on palpation
- Bi-basal end inspiratory lung crackles
- Finger clubbing small pleural effusions
45
end stage for many ILD
pulmonary fibrosis- irreversible lung disease
- collagen fibrosis damages bronchioles and alveoli- greatly decreased gas exchange
- increase fibroblast activity
46
cause sof ILD
- Specific exposure e.g. asbestosis drugs, mouldy hay
- Autoimmune- mediated inflammation (fibroblast activity)
- Unknown injury (idiopathic pulmonary fibrosis)
47
interstitial lung disease- lung elastic recoil vs chest wall elastic recoil in Diffuse Pulmonary Fibrosis
- With fibrosis tissue in the lung interstitial
- Lungs are stiff and hard to expand- lower compliance
- Lung elastic recoil is greater and the lung volume is smaller compared to normal lungs
48
example of occupational ILD
asbestosis
| coal workers pneumociosis
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example of treatment ILD
```
radiation
methotrexate
nitrofurotoin
amiodarone
chemo
```
50
example of connective tissue disorder ILD
SLE
| Rh. arthritis
51
example of immunological ILD
sarcoidosis
| ext. allergic alveilititis
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example of idiopathic ILD
fibrosing alveilititis (IPF/ CFA)
53
neonatal resp distress syndrome
- Preterm babies <37
o Insufficient surfactant- high surface tension
o The lungs are stiff
Lung expansion at birth is incomplete
o Some alveoli remain collapsed (airless) – no gas exchange occurs in these alveoli
Increased effort is required to breathe- respiratory difficult
54
In preterm babies (severe < 30 weeks) Features of respiratory difficulty from birth
```
Ø Grunting,
Ø Nasal flaring,
Ø Intercostal and subcostal retractions
Ø Rapid respiratory rate (tachypnoea)
Ø Cyanosis
```
55
surfactant production by type II alveolar cells starts at
24-28 weeks gestation
o Increasing amounts by 32 weeks
o Usually sufficient by 35-36 weeks
56
Neonatal respiratory distress syndrome vs PF
- Both have stiff lungs
- Both decreased compliance and increased elastic recoiled
- Diff underlying mechanisms
57
Chronic obstructive pulmonary disease (COPD)
- Third leasing cause of death worldwide- worldwide prevalence 10%
- Primarily caused by smoking and/or inhalation pollutants interacting with genetic vulnerability
- Clinical syndrome characterised by chronic respiratory symptoms with associated pulmonary abnormalities- all conditions share impaired airflow that is not reversible
58
COPD encompasses 2 conditions
o Chronic bronchitis
| o Emphysema
59
o Chronic bronchitis
o Emphysema
usually
co-exist
60
pre-COPD
COPD relatively new term- airflow impaired but no clinical symptoms yet and normal spirometry- but at very high risk of COPD in next 5 years
- often underdiagnosed
- should be recognised earlier
61
COPD- chronic bronchitis
- From bronchi to bronchioles
- Mucous hypersecretion (from goblet and sub mucu glands)
- Reduced cilia- mucus not cleared
- Effect of above leads to
o airflow limitation/ obstruction of small airways- worse on expiration
o Epithelial remodelling
o Alteration of airway surface tension predisposing to collapse
62
clinical diagnosis of COPD
cough productive sputum
| o 3 months of the year >one year
63
emphysema
- Air sacs disease
- Abnormal permanent enlargement of the air spaces distal to the terminal bronchiole
- With destruction of alveolar walls (no fibrosis)
- Inflammatory cells accumulate- which release elastase sand oxidants destroy alveoli walls and elastin
- Protease mediated destruction of elastin
- Reduced elastic recoil is a key problem- airway trapping
- Reduced surface area for gas exchange
64
what phenomenon is recongised to be a sign of emohysema
Barrel chest
65
Barrel chest
In a normal adult chest, the ratio of anteroposterior to transverse (or lateral) diameter is 1:2. In patients with barrel chest, this ratio approaches 1:1 as the anteroposterior diameter enlarges.
Increased air traffic and imbalance between the elastic recoil of the chest wall and the elastic recoil of the lungs- increased compliance and decreased elastic recoil- increased lung volume
66
Both emphysema and PF are disorders of ventilation- but different problems with airflow : emphysematous dominant COPD
- loss of elastic tissue
- increased compliance and reduced elastic recoil
- hyper- inflated: barrel chest
- small airways collapse in expiration (loss of radial traxtion)
- air trapping (because of obstruction and decreased recoil)
- obstructive pattern on spirometry testing
67
Both emphysema and PF are disorders of ventilation- but different problems with airflow : pulmonary fibrosis
- increase if fibrous tissue
- less compliant- harder to expand
- smaller lungs
- decreased functional residual capacity and other lung volume
- no airway obstruction- restrictive disease on spirometry tresting
68
pneumothorax
simply- presence of air in intrapleural space
- If the chest wall or the lung is breached
- A communication is created between pleural space and atmosphere
- Air flows from atmosphere (higher pressure) into the pleuracavity (lower pressure)
- Until the pleural pressure = atmospheric pressure
69
properties of the pneumothorax
- Pleural seal is lost
- Lung elastic recoil not counter-balanced by negative pleural pressure
- Lung collapses to unstretched size
70
hypoventilation
failure to breath rapidly enough or deep enough
71
hypoventilation brainstem
opiates, head injury
72
hypoventilation spinal cord
truama
73
hypoventilation phrenic and intercosta nerves
guillain-barre syndrome
74
hypoventilation NMJ
myasthenia gravis
75
hypoventilation muscles of resp
inherited diseases (duchennes muscular dystrophy)
76
hypoventilation chest wall
severe obesity, kyphoscoliosis, flail segment
77
hypoventilation pleural cavity
pneuomthorax
78
hypoventilation poor lung compliance
res distress of new born, fibrosis
79
hypoventilation upper airway obsturction
laryngeal oedema, foreign body
80
hypoventilation high airway resistance
very severe acute asthma, late stage of COPD
81
Normal cough involves the following steps
- Deep inspiration
- The glottis is closed by vocal cord adduction
- Strong contraction of the expiratory muscles (abdominal muscles, internal intercostal muscles) which build up with intrapulmonary pressure
- Sudden opening of the glottis causes an explosive discharge of air
82
The cough reflex
‘explosive expiration of air from the lungs’
- Cough reflex is co-ordianted by cough centre in the medulla oblongata
- Initiated by irritation of mechano- and/or chemoreceptors in the respiratory epithelium
83
anatomical dead space
volume of air in the conducting airways
84
alveolar dead space
air in alveoli which do not take part in gas exchange (these are alveoli which are not perfused or are damaged)
85
physiological dead space
anatomical dead space and alveolar dead space
86
tidal volume=
anatomical dead space + alveolar ventilation
87
total pulmonary ventilation (mnute volume)=
tidal volume X respiratory rate
88
alveolar ventilation =
(tidal volume - dead space) x resp rate
