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Respiratory > Clinical application of lung ventilation > Flashcards

Clinical application of lung ventilation Flashcards

1
Q

Outline how ventilation takes place

A
  • Inspiratory muscles contract
  • Chest expands, taking lung with it (pleural seal)
  • Air flows in, overcoming airways resistance
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2
Q

What do the lungs need to do in order to expand?

A
  • Overcome elastic properties of alveolar walls
  • Overcome surface tension of fluid
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3
Q

What is quiet expiration?

A
  • Passive process
  • Needs elastic recoil of lungs
  • Need to overcome airways resistance
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4
Q

What is COPD?

A
  • 3rd leading cause of death worldwide
  • Primarily caused by smoking and/or inhaled pollutants with genetic vulnerability
  • Clinical syndrome characterised by chronic respiratory symptoms with associated pulmonary abnormalities
  • All conditions share impaired airflow that is not fully reversible
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5
Q

Why is COPD greatly underdiagnosed?

A
  • COPD may start in people in their 30s though typical age of presentation is in the 60s
  • Should be recognised earlier
  • Earlier intervention slows lung function decline
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6
Q

Which 2 lung conditions often exist in COPD?

A
  • Chronic bronchitis and emphysema
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7
Q

What does emphysema affect?

A
  • affects spaces distal to terminal bronchiole
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8
Q

Where does chronic bronchitis affect the lungs?

A
  • Seen in larger airways
  • Results in mucus hypersecretion from goblet cells and sub-mucous glands
  • Reduced cilia - mucociliary escalator function impaired
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9
Q

Compare cartilage in small bronchi vs bronchioles

A
  • Small bronchi have small islands of cartilage
  • Bronchioles have no cartilage
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10
Q

Compare glands in small bronchi vs bronchioles

A
  • Small bronchi have glands in the submucosa
  • Bronchioles have no glands
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11
Q

What keeps the lumens of the bronchioles open?

A
  • No cartilage
  • Radial traction (outward tugging) of surrounding alveolar walls on bronchioles
  • Prevents collapse of bronchioles during expiration
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12
Q

What is the definition of emphysema?

A
  • Abnormal, permanent enlargement of air spaces distal to terminal bronchiole
  • With destruction of alveolar walls
  • No fibrosis
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13
Q

Outline the pathophysiology of emphysema

A
  • Protease mediated destruction of elastin
  • Loss of elastic tissue
  • Compliance increased (more easily stretched)
  • Elastic recoil reduced (lung remains more expanded at end of expiration)
  • Damaged alveolar walls leads to loss of radial traction
  • Bronchioles collapse in expiration
  • Air trapping due to airway obstruction and decreased elastic recoil
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14
Q

What signs can be seen in a patient who is suffering from air trapping due to emphysema?

A
  • Hyper inflated: barrel chest
  • Obstructive pattern on spirometry
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15
Q

What happens to the bronchioles in COPD?

A
  • Walls of bronchioles and bronchi become inflamed and plugged with mucus
  • Airway resistance is increased
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16
Q

How can you tell that someone has a barrel chest?

A
  • Antero-posterior: lateral diameter diameter = 1:1
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17
Q

How can you see hyperinflation on a chest X-ray?

A
  • Diaphragm crosses 8th rib anteriorly and is flattened
  • In a normal lung, diaphragm crosses 5th rib anteriorly
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18
Q

What is the interstitium of the lungs?

A
  • Microscopic space between alveolar epithelium and capillary endothelium
  • Gas exchange occurs across interstitial layer
  • If it is damaged, gas exchange is impaired
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19
Q

What does the interstitium contain?

A
  • Elastin fibres
  • Collagen fibres
  • Fibroblasts
  • Matrix substance
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20
Q

What happens to the interstitium in pulmonary fibrosis?

A
  • Interstitium is thickened and fibrosed
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21
Q

What are some occupational interstitial lung diseases?

A
  • Asbestosis
  • Silicosis
  • Coal worker’s pneumoconiosis
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22
Q

What are some connective tissue diseases that cause interstitial lung disease?

A
  • Rheumatoid arthritis
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23
Q

What are some immunological causes of interstitial lung diseases?

A
  • Sarcoidosis
  • Ext. allergic alveolitis
24
Q

What are some immunological causes of interstitial lung disease?

A
  • Fibrosing alveolitis
25
Q

What is the pathophysiology of interstitial fibrosis?

A
  • If exposure or injury persists or if repair process is imperfect, permanent damage may occur
  • Increased interstitial tissue replacing normal capillaries, alveoli, and healthy interstitium
26
Q

What is the effect of fibrosis on the lungs?

A
  • Lung compliance is reduced - lungs are stiff; harder to expand
  • Elastic recoil of lungs is increased - resting lung volume is smaller than normal
  • Restrictive type of ventilatory defect on spirometry
27
Q

What happens to gas exchange in diffuse lung fibrosis?

A
  • Alveolar capillary membrane is thickened
  • Increases diffusion distance for O2 and CO2
  • Impairs gas exchange
28
Q

What are the symptoms of lung fibrosis?

A
  • Breathlessness on exertion/at rest
  • Dry cough
  • Relevant previous history e.g. occupation, drug history, etc.
29
Q

What are the signs of lung fibrosis?

A
  • Chest expansion is reduced
30
Q

What is the tidal volume?

A
  • Volume of air that enters and leaves lungs with each breath
31
Q

How do we further increase lung volume?

A
  • Increase lung volume to extent of inspiratory reserve volume
  • During normal quiet respiration, increase in lung volume is not maximal
32
Q

How do we breathe out more than at rest?

A
  • Use expiratory reserve volume
33
Q

Can we completely empty our lungs?

A
  • No
  • Even after forced expiration a residual volume of air remains
34
Q

What are the fixed points that lung capacities are defined relative to?

A
  • Maximum inspiration
  • Maximum expiration
  • The end of a quiet expiration
35
Q

What is vital capacity?

A
  • Inspiratory reserve volume + tidal volume + expiratory reserve volume
36
Q

What is total lung capacity?

A
  • Vital capacity + residual volume
37
Q

What is functional residual capacity?

A
  • Volume of air in lungs at the end of quiet expiration
  • Expiratory reserve volume + residual volume
38
Q

What functional residual capacity depend on?

A
  • Balance between lung elastic recoil and chest wall elastic wall recoil
  • Emphysema leads to increased FRC
  • Lung fibrosis leads to reduced FRC
39
Q

What causes neonatal respiratory distress syndrome?

A
  • Pre-term babies <35 weeks don’t produce sufficient lung surfactant
  • High surface tension
  • Lung expansion at birth incomplete
  • Some alveoli remain collapsed and no gas exchange can occur
  • Lung is stiff
  • Increased effort required to breathe - babies grunt + nasal flaring
  • Results in impaired ventilation
40
Q

What are the clinical features of NRDS?

A
  • Grunting
  • Nasal flaring
  • Intercostal and subcostal retractions
  • Tachypnoea
  • Cyanosis
41
Q

How is NRDS treated?

A
  • Surfactant replacement via endotracheal tube
  • Supportive treatment with oxygen and assisted ventilation
42
Q

What is a pneumothorax?

A
  • Pleural seal is lost
  • Lung elastic recoil not counter-balanced by negative pleural pressure
  • Air rushes in, causing lung to collapse
  • Compression collapse
43
Q

What is the balance of forces at the end of quiet expiration?

A
  • Chest wall always wants to move outwards and lungs always want to move inwards
44
Q

What happens to the balance of forces during a pneumothorax?

A
  • Chest wall or lung is breached
  • Communication is created between pleural space and atmosphere
  • Intrapleural pressure increases and allows lung to collapse
45
Q

What is a resorption collapse?

A
  • Collapse due to obstruction of a large airway
46
Q

What is atelectasis?

A
  • Alveoli not ventilated so can’t participate in gas exchange
  • Collapsed alveoli more susceptible to lung infection including pneumonia
  • Common post-operative complication
  • Prevent with good pain control to enable coughing/clearance of mucus, deep breathing exercises, early ambulation
47
Q

What affects the brainstem to cause hypoventilation?

A
  • Opiates
  • Head injury
48
Q

What affects the spinal cord to cause hypoventilation?

A
  • Trauma
49
Q

What affects the phrenic and intercostal nerves to cause hypoventilation?

A
  • Guillain-Barre syndrome
50
Q

What affects the neuromuscular junction to cause hypoventilation?

A
  • Myasthenia gravis
51
Q

What affects the muscles of respiration to cause hypoventilation?

A
  • Inherited muscle diseases e.g. Duchenne muscular dystrophy
52
Q

What affects the chest wall to cause hypoventilation?

A
  • Severe obesity
  • Kyphoscoliosis
  • Flail segment
53
Q

What affects the pleural cavity to cause hypoventilation?

A
  • Pneumothorax
  • Large pleural effusions
54
Q

What affects lung compliance to cause hypoventilation?

A
  • Respiratory distress of newborn
  • Lung fibrosis in interstitial lung disease
55
Q

What affects the upper airway to cause hypoventilation?

A
  • Obstruction due to laryngeal oedema or foreign body
56
Q

What affects airway resistance to cause hypoventilation?

A
  • High airway resistance due to very severe acute asthma or late stages of COPD
57
Q

What affects airway resistance to cause hypoventilation?

A
  • High airway resistance due to very severe acute asthma or late stages of COPD

Respiratory (21 decks)

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