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Respiratory > Lecture 4- Clinical application in ventilation and lung mechanics > Flashcards

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
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2
Q

resp portion

A

resp bronchioles
alveolar ducts
alveoli

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3
Q

alveoli made up of

A

type 1 pneumocytes- gas exchange

type 2 pneumocytes- surfactant

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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

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5
Q

QUIET EXPIRATION

A

• Passive process:
– Needs elastic recoil of Lungs
– Need to overcome airways resistance

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6
Q

compliance is a measure of

A
  • Compliance is a measure of distensibility- change in volume relative to change in pressure
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7
Q

e.g. low compliance in

A

brand new balloon

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8
Q

e.g. high compliance in

A

older balloon (easier to blow up)

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9
Q

elastance is a measure of

A

elastic recoil

the tendency of something that has been distended to return to its original size

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10
Q

o In tissue with high compliance

A

easier to stretch, elastic recoil is less

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11
Q

o In tissues with low compliance

A
  • elastic recoil is high (tendency to return to original size)
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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)

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13
Q

E.g. the higher the compliance (the more distensible)

A

the worse the elastic recoil – e.g. go back to original shape

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14
Q

E.g. the lower the compliance (less distensible- harder to inflate)

A

the better the elastic recoil e.g. lung fibrosis

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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
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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

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17
Q

the more elastic fibres in the connective tissue surrounding the alveoli

A

the lower the compliance- harder to inflate lungs

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18
Q

The greater the alveolar surface tension, the

A

lower the lung compliance. (inversely related)

o Surfactant decreases surface tension, therefore increasing compliance

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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)

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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

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21
Q

lung elastic recoil is inversely related to

A

lung compliance

0 the higher the compliance, the less elastic recoil

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22
Q

small bronchus have

A

small islands of cartilage and glands in submucosa

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23
Q

bronchioles have

A

no caritlage or no glands

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24
Q

how do bronchioles stay open on expiration if they have no cartilage

A

radial traction

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25
Q

radial traction

A

outward tugging action of the surrounding alveolar wall on bronchioles- tether them open
- Prevents collapse of bronchioles on expiration

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26
Q

Why is airway obstruction worse in expiration than inspiration?

A
  • 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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27
Q

ATELECTASIS

A

– lung collapse – several causes

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28
Q

INTERSTITIAL LUNG DISEASE

A

Lung expansion difficult secondary to stiff lungs from increased collagen in
alveolar walls – decreased compliance

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29
Q

HYPOVENTILATION

A
  • Inability to expand chest- many causes
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30
Q

PNEUMOTHORAX

A
  • Air in the pleural space with loss of pleural seal
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31
Q

OBSTRUCTIVE LUNG DISEASE (COPD&ASTHMA)-

A

↑airways resistance and, in emphysema decreased elastance secondary to loss elastin – compliance actually increased

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32
Q

RESPIRATORY DISTRESS SYNDROME NEW BORN -

A

↓ surfactant leads to increased surface tension and decreased compliance

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33
Q

in simple terms atelectasis is the inadequate expansion of air space- alveolar collaps and has 3 causes

A
  • 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
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34
Q

Compression collapse: due to:

A 
o	Air in pleural cavity (pneumothorax)
	Air
	Liquid
	Tumour
o	Fluid in the pleura
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35
Q
  • Resorption collapse: due to obstruction
A

o Airway obstructed; air downstream of blockage slowly absorbed into blood stream= empty alveolar = collapse

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36
Q

How does atelectasis it cause impaired respiratory function?

A
  • 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
Q

resportion collapse

A

Resorption collapse

- Due to obstruction of large airway e.g. lung cancer, mucous plugs

38
Q

interstitial lung disease

A

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
Q

thickening of the pulmonary interstitium in ILD is caused by

A

too many elastic fibres

- alveoli have reduced compliance and wont inflate

40
Q

histology in ILD

A

shows thickening of intersitium between alveoli

41
Q

ILD also affects

A

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
Q

Features of ILD

A
  • 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
Q

Clinical symptoms of ILD

A
  • Dry cough
  • Dyspnoea (short of breath) on exertion progressing to at rest
  • Fatigue
  • Typically gradual, insidious progression Sx
44
Q

Signs of ILD

A
  • Decreased lung excursion on palpation
  • Bi-basal end inspiratory lung crackles
  • Finger clubbing small pleural effusions
45
Q

end stage for many ILD

A

pulmonary fibrosis- irreversible lung disease

  • collagen fibrosis damages bronchioles and alveoli- greatly decreased gas exchange
  • increase fibroblast activity
46
Q

cause sof ILD

A
  • Specific exposure e.g. asbestosis drugs, mouldy hay
  • Autoimmune- mediated inflammation (fibroblast activity)
  • Unknown injury (idiopathic pulmonary fibrosis)
47
Q

interstitial lung disease- lung elastic recoil vs chest wall elastic recoil in Diffuse Pulmonary Fibrosis

A
  • 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
Q

example of occupational ILD

A

asbestosis

coal workers pneumociosis

49
Q

example of treatment ILD

A 
radiation
methotrexate
nitrofurotoin
amiodarone
chemo
50
Q

example of connective tissue disorder ILD

A

SLE

Rh. arthritis

51
Q

example of immunological ILD

A

sarcoidosis

ext. allergic alveilititis

52
Q

example of idiopathic ILD

A

fibrosing alveilititis (IPF/ CFA)

53
Q

neonatal resp distress syndrome

A
  • 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
Q

In preterm babies (severe < 30 weeks) Features of respiratory difficulty from birth

A 
Ø Grunting,
Ø Nasal flaring,
Ø Intercostal and subcostal retractions 
Ø Rapid respiratory rate (tachypnoea) 
Ø Cyanosis
55
Q

surfactant production by type II alveolar cells starts at

A

24-28 weeks gestation
o Increasing amounts by 32 weeks
o Usually sufficient by 35-36 weeks

56
Q

Neonatal respiratory distress syndrome vs PF

A
  • Both have stiff lungs
  • Both decreased compliance and increased elastic recoiled
  • Diff underlying mechanisms
57
Q

Chronic obstructive pulmonary disease (COPD)

A
  • 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
Q

COPD encompasses 2 conditions

A

o Chronic bronchitis

o Emphysema

59
Q

o Chronic bronchitis
o Emphysema

usually

A

co-exist

60
Q

pre-COPD

A

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
Q

COPD- chronic bronchitis

A
  • 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
Q

clinical diagnosis of COPD

A

cough productive sputum

o 3 months of the year >one year

63
Q

emphysema

A
  • 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
Q

what phenomenon is recongised to be a sign of emohysema

A

Barrel chest

65
Q

Barrel chest

A

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
Q

Both emphysema and PF are disorders of ventilation- but different problems with airflow : emphysematous dominant COPD

A
  • 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
Q

Both emphysema and PF are disorders of ventilation- but different problems with airflow : pulmonary fibrosis

A
  • 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
Q

pneumothorax

A

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
Q

properties of the pneumothorax

A
  • Pleural seal is lost
  • Lung elastic recoil not counter-balanced by negative pleural pressure
  • Lung collapses to unstretched size
70
Q

hypoventilation

A

failure to breath rapidly enough or deep enough

71
Q

hypoventilation brainstem

A

opiates, head injury

72
Q

hypoventilation spinal cord

A

truama

73
Q

hypoventilation phrenic and intercosta nerves

A

guillain-barre syndrome

74
Q

hypoventilation NMJ

A

myasthenia gravis

75
Q

hypoventilation muscles of resp

A

inherited diseases (duchennes muscular dystrophy)

76
Q

hypoventilation chest wall

A

severe obesity, kyphoscoliosis, flail segment

77
Q

hypoventilation pleural cavity

A

pneuomthorax

78
Q

hypoventilation poor lung compliance

A

res distress of new born, fibrosis

79
Q

hypoventilation upper airway obsturction

A

laryngeal oedema, foreign body

80
Q

hypoventilation high airway resistance

A

very severe acute asthma, late stage of COPD

81
Q

Normal cough involves the following steps

A
  • 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
Q

The cough reflex

A

‘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
Q

anatomical dead space

A

volume of air in the conducting airways

84
Q

alveolar dead space

A

air in alveoli which do not take part in gas exchange (these are alveoli which are not perfused or are damaged)

85
Q

physiological dead space

A

anatomical dead space and alveolar dead space

86
Q

tidal volume=

A

anatomical dead space + alveolar ventilation

87
Q

total pulmonary ventilation (mnute volume)=

A

tidal volume X respiratory rate

88
Q

alveolar ventilation =

A

(tidal volume - dead space) x resp rate

Respiratory (27 decks)

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