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Physiology- CP > Pulmonary Mechanics > Flashcards

Pulmonary Mechanics Flashcards

1
Q

Describe the movement of the diaphragm in ventilation

A
  • Flat sheet of skeletal muscle fixed at edge of thoracic wall
  • Separates abdomen from thorax
  • At rest- concave
  • Phrenic nerve somatic innervation
  • Fibres shorten and flatten, increasing volume of thoracic cavity
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2
Q

Describe the movement of the thoracic wall

A
  • Various skeletal muscles move ribs
  • Outwards for inspiration
  • Inwards for expiration
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3
Q

Which muscles contract during inspiration?

A
  • Diaphragm
  • External intercostal muscle
  • Shoulder girdle muscles
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4
Q

Which muscles contract during expiration?

A
  • Internal intercostal muscles

- Abdominal wall muscles

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5
Q

Why does inspiration need muscle activity?

A
  • Requires muscle activity to overcome elastic tissue of lungs
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6
Q

What occurs in airways during inspiration?

A
  • Breathing in draws airways open
  • As lung volume increases, airways are pulled by inflation
  • From middle outwards- radial traction
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7
Q

Why can expiration be passive down to FRC?

A

Due to natural elastic recoil of thoracic and lung tissue

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8
Q

In what circumstances are expiratory muscles needed?

A
  • To go below FRC
  • To achieve high pressures
  • To achieve high flow rates (flow limitation due to dynamic collapse of airways)
  • Forced expiration
  • Smoking
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9
Q

How are expiratory muscles used in forced expiration?

A
  • Increased pressure flattens small airways, flow limitation

- Airways are connected together- interdependence which prevents collapse

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10
Q

Why are expiratory muscles used more in smokers?

A
  • Smoking causes neutrophils flooding which may lead to emphysema
  • This means more muscle activity is required for adequate ventilation
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11
Q

How does elastic recoil occur?

A
  • Elastic properties of tissue

- Also by surface tension of air-fluid interface in alveoli

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12
Q

What are the functions of elastic fibres?

A
  • Elastic recoil

- Keeping small airways without cartilage open

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13
Q

What secretes pulmonary surfactant?

A
  • Alveolar type 2 cellS
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14
Q

What is pulmonary surfactant?

A
  • Covers the surfaces of alveoli

- Helps expiration

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15
Q

What two pressures contribute to alveolar pressure?

A

Alveolar pressure is the sum of

  • Pressure acting on outside alveolus
  • Pressure generated by elastic recoil of alveolus
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16
Q

What is pleural pressure determined by?

A

Muscular effort

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17
Q

How can pleural pressure me measured?

A

By passing a balloon into the oesophagus

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18
Q

How can stretch ability of the lungs be expressed as?

A

Compliance

- This can be altered in some disease

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19
Q

What is the relationship between elastic recoil and lung volume?

A

Elastic recoil pressure will increase as lung volume increases

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20
Q

Why does an increase in peak flow with lung volume occur?

A
  • Elastic recoil increases with volume

- Airways have a lower resistance at larger lung volumes due to increased outward radial traction as lung expands

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21
Q

Why does flow limitation occurs?

A
  • Resistance to flow determines air flow

- This is affected by the diameter of small airways

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22
Q

Describes how forced expiration might cause airway collapse

A
  • Higher pressure in alveoli
  • Less in airways further down
  • Once pressure in airways is less than pressure in pleural cavity, airway flattens and pressure inside airway becomes less than outside
  • Pressure continuously builds up in alveoli
  • Leads to airway flutter
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23
Q

What does airway flutter lead to?

A

Airway collapse

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24
Q

How might a smoker overcome airway flutter?

A
  • Overcome by pursing lips (pink puffer)
  • Reduces pressure inside the mouth
  • Trying to move ‘critical closing point’ of airway to part that is held open by cartilage
  • Normal ventilation is maintained
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25
Q

What is a characteristic of all obstructive orders?

A
  • Low maximal expiratory flow rates
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26
Q

What diseases might affect inspiration?

A 
Abnormally stiff lungs
- Fibrosis and pulmonary oedema
Respiratory apparatus damaged
- Chest wall trauma
- Neuromuscular disease
27
Q

Where does airway resistance come from?

A
  • Mainly from upper airways

- In smaller airways, ir=t is decreased at high lung volumes

28
Q

What might increase airway resistance?

A
  • Contraction of smooth muscle (bronchoconstriction)
  • By swelling of the airway wall
  • By excretions/exudations
29
Q

Where is lung compliance decreased?

A
  • Restrictive conditions such as asbestosis or fibrosis

- When lung vascular pressure is raised like in left heart failure

30
Q

When is lung compliance increased?

A
  • In emphysema
  • Partly as a result of elastin
  • Possibly due to loss of surface area, and therefore some of surface tension
31
Q

Describe emphysema

A
  • ‘Floppy’ lungs- due to loss of elastic tissue
  • Very compliant as inflation occurs to dramatically high volumes
  • Difficult to breathe out
32
Q

Describe left heart failure

A
  • Lungs engorge with blood and oedema fluid in interstitial
  • Become stiff and non-compliant
  • When people lie supine
33
Q

Describe the composition of surfactant

A
  • 90% lipid
  • 70-80% Phosphatidylcholine
  • Lipids are stored intracellularly as lamellar bodies
34
Q

What are the mechanical functions of surfactant?

A
  • Lowers surface tension to 0 at FEC
  • Less effect as it is stretched at larger lung volumes
  • Enables small alveoli to stabilise when communicating with larger ones
  • Reduces oedema formation
35
Q

What are the consequences of having a lack of surfactant?

A
  • RDS

- In new-borns, common in premature babies as foetal surfactant develops late in gestation

36
Q

Which mechanoreceptors control ventilation?

A
  • Limbs- feet-forward stimulation of ventilation in exercise
  • Chest wall
  • Airways
  • Pulmonary vascular system
37
Q

Where are mechanoreceptors found in the chest wall?

A
  • Costo-vertebral joints
  • Respiratory muscle spindle
    (NOT in diaphragm)
  • Golgi tendon organs
38
Q

What do central chemoreceptors do in ventilation control?

A
  • Detects changes in CSF pH and provide most of normal CO₂ response
  • Raised arterial PCO₂ can lead to desensitisation to mechanism of chemical control of ventilation
  • Patient shifts into hypoxic drive
39
Q

What happens when patient shifts into hypoxic drive?

A
  • Drive to breathe comes from low arterial PO₂
  • If supplementary oxygen given, arterial PO₂ will improve but ventilation will be suppressed and arterial PCO₂ may rise dangerously
40
Q

Where are peripheral chemoreceptors found?

A
  • Aortic and carotid bodies

- Not sinus

41
Q

What is the role of peripheral chemoreceptors in ventilation control?

A
  • Normally contribute little to respiratory chemosensory drive
  • Vital when central CO₂ sensitivity lost
  • Responds very rapidly, but have a very non-linear response curve under normocapnic conditions
  • In hypercapnia, becomes more sensitive and more linear, therefore more vital
42
Q

Describe restrictive lung diseases

A
  • Usually involves decreased lung compliance (i.e. ‘small lungs’
  • Restricting inflation but increasing expiratory drive
  • May also involve impaired gas diffusion (fibrosis)
43
Q

Describe obstructive lung diseases

A
  • Impaired airflow, especially in expiration
  • May involve airway narrowing and/or obstruction
  • Or loss of elastic recoil
44
Q

Which type of lung disease is more common? (obstructive or restrictive)

A

Obstructive

45
Q

Describe what is meant by ‘shortness of breath’

A
  • Clinically defined as ‘an awareness of breathing’
  • May result from increased ventilation with exercise/disease
  • Often arises from disparity between effort put into breathing and result in terms of chest movement or lung inflation
  • May arise from stimulation of lung
46
Q

Why might restrictive lung disorders occur?

A
  • Exposure to chronic allergens or irritants

- Often results in interstitial lung disease with infiltration and scarring of lung (fibrosis)

47
Q

How might restrictive lung disorders affect ventilation?

A
  • May cause diffusion impairment, especially on exercise

- Breathlessness with exercise

48
Q

What is asthma?

A

Obstructive respiratory disease characterised by airway resistance due to inflammation and broncho-constriction

49
Q

What is asthma presentation like?

A

Episodic

50
Q

Describe airway resistance in asthma

A
  • Less in inspiration than expiration

- Ratchet-like effect on lung volumes which may increase greatly during an attack

51
Q

What occurs in the lungs in emphysema?

A
  • Enlargement of air spaces distal to terminal bronchiole
  • Excessive protease activity- smoking-induced neutrophil
  • Loss of alveolar walls and related capillary bed
  • Loss of elastic recoil- reduced SA- loss of surface tension component
  • Loss of radial traction- increased airway collapse on expiration- air trapping
  • Chronic over-inflation- increased TLC, RV, FRC
  • Decreased VC, FEV1 and ratio
52
Q

What is an observable characteristic of emphysema?

A

Dyspnoea/breathlessness

53
Q

What is bronchitis?

A
  • Chronic over-production of mucus in bronchial tree
  • With periods of infection and excessive expectoration
  • On most days for at least 3 months in 2 successive years constitutes as chronic bronchitis
  • Usually co-exists with emphysema in COPD
54
Q

What happens to mucus glands in bronchitis

A
  • Hypertrophy
  • Chronic inflammatory changes in larger airway walls
  • Inflammatory cell infiltration
  • Oedema of walls
55
Q

What happens to lung volumes in chronic bronchitis?

A
  • Reduced FEV1, FCV, FEV1:FVC ratio
56
Q

What is a significant characteristic of bronchitis?

A

Productive cough

57
Q

Describe COPD

A
  • Chronic Obstructive Pulmonary Disease
  • Smokers
  • Features of bronchitis and emphysema in varying proportion
58
Q

What are the two broad presentations of COPD

A

Blue bloater and pink puffer (first will often progress into the second)

59
Q

Describe what is meant by ‘pink puffer’

A
  • Better oxygenation
  • Normal PCO₂
  • More dyspnoea
  • More emphysematous spirometric changes
60
Q

Describe what is meant by ‘blue bloater’

A
  • Hypoxemic
  • Cyanotic
  • Hypercapnic
  • Sluggish and drowsy
  • Right heart failure
61
Q

Describe the Dynamic Respiratory Test

A
  • Breathe out as hard and fast as they can
  • Volume of gas breathed out- forced vital capacity
  • How much breathed out in one second (FEV1)- anything above 70% is normal
62
Q

What are the results of a test for someone with an obstructive disease?

A
  • Cannot breathe in as much (vital capacity is low)

- Slow expiration- low FEV1

63
Q

What are the results of a test for someone with an restrictive disease?

A
  • Lungs behave normally

- Small amounts for FEV or FVC

64
Q

What is forced expiratory time as a lung assessment?

A
  • Time taken for expiration

- Severe obstructive diseases lead to long FET

Physiology- CP (19 decks)

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