Clinical Pplication Of Lung Mechanics

Question 1

What is the roles fo mucks and cilia

Answer 1

Dust and other particles inhaled with air • Large particles
• filtered in nose;
• deposited on mucus layer in nose, nasopharynx, swept by cilia  to oropharynx
swallowed
• Medium sized particles
• Deposited on mucus lining the trachea, bronchi and larger bronchioles
• Wafted up to pharynx by cilia (muco-ciliary escalator)  swallowed
• Small (1 – 5 µm)
• Carried down to alveoli
• Engulfed by macrophages  removed by lymphatics and via airways (muco-ciliary)

Question 2

Decisive teh histology of bronchioles

Answer 2

See slide

Question 3

What is radial traction

Answer 3

Radial traction
• term used for the outward tugging action of the alveolar walls on bronchioles
• prevents collapse of bronchioles during expiration

Question 4

What are compliance and elastase

Answer 4

Compliance - how stretchy it is
Elastance = meagre of elastic recoil - returning to original size

Compliance is proportional to 1/elastance

Question 5

What is teh interstitum?

Answer 5

The microscopic space between the alveolar epithelium and capillary endothelium

Question 6

What does the interstitial contain?

Answer 6

Interstitium contains:
• elastin fibres,
• collagen fibres
• fibroblasts

Question 7

What is interstitial lung disease (diffuse lung fibrosis)?

Answer 7

Fibrous tissue in the interstitium • Lungs are stiff so harder to expand • lung compliance is lower
• Elastic recoil of the lungs is increased
• The lung volume is lower than normal
• 0Restrictive’ type of ventilatory defect

Question 8

What causes interstitial lung disease

Answer 8

Can follow
• a specific exposure - e.g., asbestos, drugs, mouldy hay etc
• autoimmune-mediated inflammation
• Unknown injury (e.g., idiopathic pulmonary fibrosis)

• If the exposure or injury persists or if the injury repair process is imperfect, the lung may be permanently damaged
• with increased interstitial tissue replacing the normal capillaries, alveoli, and healthy interstitium.

Question 9

What is functional residual capacity

Answer 9

FRC = Functional residual capacity

The volume of air in the lungs at the end of a quiet expiration

Question 10

What are the symptoms of interstitial lung diesease

Answer 10

Symptoms • Breathlessness 
• Dry cough 
• Relevant previous history:
occupation, drug history, etc
Signs
Chest expansion is ???

Question 11

What happens to gas exchange in interstitial lung disease

Answer 11

In the normal lung: air in alveoli lies as close as 0.2μm from blood streaming through capillaries.
2 2
In interstitial lung disease (diffuse lung fibrosis) • alveolar capillary membrane is thickened • Increases diffusion distance for O • Impairs gas exchange (more next week)
and CO
(Diffusion defect)

Question 12

What is emphysema

Answer 12

Definition:
• Abnormal, permanent enlargement of the air spaces distal to the terminal bronchiole
• With destruction of alveolar walls
(No fibrosis)

Protease mediated destruction of elastin is an important feature
Reduced elasticity is a key problem
Large air spaces -> reduced surface area for gas exchange

Question 13

What can cause emphysema?

Answer 13

Due to
• Smoking and inhaled pollutants, (COPD is commonest cause)
cause inflammatory cells to accumulate; which release elastases and oxidants -> destroy alveolar walls and elastin
• Most have chronic bronchitis concurrently (since smoking is a risk factor for both).

Question 14

What is COPD

Answer 14

Chronic Obstructive Pulmonary disease (COPD) = umbrella term including both
Emphysema + chronic bronchitis
Larger airways - chronic bronchitis
Smaller airways and alveoli - emphysema .

Most ppl with emphysema have chronic bronchitis too

Question 15

Where is chronic bronchitis usually sen

Answer 15

• Chronic bronchitis is seen in the larger airways
• Mucus hypersecretion (from goblet cells & sub mucous glands)
• Reduced cilia – mucus is not cleared effectively

Question 16

Why is airway obstriction worse in expiration than inspiration

Answer 16

Inspiration 0 negative pressure in pleural space during inspiration helps to keep he lower airways open

Positive intra pulmonary pressure during expiration exacerbates narrowing of intrathoracic airways

Question 17

Describe the chanegs in emphysema

Answer 17

• Loss of elastic tissue
• Elastic recoil is decreased.
• Compliance increased
• Small airways collapse in expiration (loss of radial traction)
• Air trapping (due to airway obstruction and low elastic recoil )
• Hyper inflated: Barrel chest
• obstructive pattern on spirometry testing

Question 18

What is a barrel chest

Answer 18

Normal: ratio of Antero-posterior : lateral diameter = 1:2

Barrel chest: Antero-posterior : lateral diameter = 1:1

Question 19

Compare the X-rays of normal lungs and emphysema

Answer 19

Normal inflation vs hyper inflation
Normal - diaphragm crosses 5th rib anteriorly
Emphysema - diaphragm crosses 8th rib anteriorl, diaphragm flattened
See slide

Question 20

How does pneumothorax occur

Answer 20

• 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 pleural cavity (lower pressure)
• Until the pleural pressure = atmospheric pressure
• The pleural seal is lost
• Lung elastic recoil not counter-balanced by negative pleural pressure
• Lung collapses to unstretched size
Chest drain with underwater seal used

Question 21

What is atelectasis

Answer 21

Atelectasis (lung collapse) Inadequate expansion of air spaces
• In new-born babies: failure of alveoli to expand at birth
• Compression collapse: due to
• air in pleural cavity (pneumothorax)
• fluid in the pleural cavity (pleural effusion)
• Resorption collapse: due to obstruction
Airway obstructed; air downstream of
blockage slowly absorbed into blood stream

Question 22

What is resorption collapse

Answer 22

Collapse due to obstruction of a large airway (eg Lung cancer, mucus plugs)

Question 23

What is neonatal respiratory distress syndrome

Answer 23

Surfactant
• Produced by Type II alveolar cells; starts at 24 – 28 weeks gestation;
• increasing amounts by 32 weeks
• Usually sufficient by 35 – 36 weeks
In preterm babies Insufficient surfactant -> high surface tension lung expansion at birth is incomplete; some alveoli remain collapsed (airless); no gas exchange occurs in these alveoli
The lung is stiff Increased effort is required to breathe – respiratory difficulty Results in impaired ventilation

Question 24

What are some features of respirate difficulty from birth and what are some treatments

Answer 24

In preterm babies (severe  < 30 weeks) • Features of respiratory difficulty from birth
• grunting,
• nasal flaring,
• intercostal and subcostal retractions
• Rapid respiratory rate (tachypnea)
• cyanosis

• Treatment includes
• surfactant replacement via an endotracheal tube,
• supportive treatment with oxygen and assisted ventilation