Lecture 2 - Clinical Application in Lung Ventilation

Question 1

What is COPD and what is it primarily caused by?

Answer 1

• Clinical syndrome encompassing 2 conditions - chronic bronchitis and emphysema.
• Primarily caused by smoking/inhaling pollutants which interact w/a genetic vulnerability

Question 2

What is chronic bronchitis and what effects does it have on the respiratory tract?

Answer 2

• Disease of small airways, chronic inflammation in small bronchi and bronchioles.
• Mucous hyper-secretions (goblet cells), reduced cilia and clearance, epithelial remodelling, increased airway surface tension. Leads to increased air flow resistance + therefore compliance as inflammation and increase mucous massively reduce airway diameter.

Question 3

Describe the pathophysiological basis of emphysema & what its effect on elastic recoil is.

Answer 3

• Abnormal permanent enlargement of air spaces distal to terminal bronchiole. Inflammatory cells accumulate destroying alveolar walls and elastin (due to release of elastases) reducing elastic recoil.
• Therefore harder to exhale + leads to collapsing of small airways

Question 4

A bronchiole has no cartilage (whereas a bronchus does). How do bronchioles therefore stay open in expiration?

Use this to explain why people with COPD get bronchioles collapsing early during expiration

Answer 4

• Due to radial traction (outward tugging action of surrounding alveolar walls).
• COPD patients lose alveoli, meaning less radial traction + collapsing of bronchioles

Question 5

Why do patients with emphysema often end up with a barrel chest?

Answer 5

• Elastic recoil decreased, compliance increased. FRC therefore increased, air becomes trapped flattening the diaphragm, leading to barrel chest.

Question 6

Therefore, summarise the airway obstructive effects of COPD.

Answer 6

• Small airways narrowed due to inflammation of bronchiolar periphery, luminal occlusion by mucous and reduced radial traction via disruption of alveolar attachments (emphysema).

Question 7

Describe the pathophysiological basis of atelectasis (lung collapse)

Describe the common causes of compression and resorption atelectasis.

Answer 7

• Impaired pulmonary surfactant production, alveoli collapse secondary to increased surface tension.

Compression (pressure on alveoli) - pneumothorax, pleural effusion, abdominal obesity, post GI surgery

Resorption (due to obstruction) - airways obstructed by blockage e.g.: lung cancer or mucous plugs

Question 8

What are the end consequences of atelectasis

Answer 8

• Alveoli not ventilated, can’t participate in gas exchange (impaired oxygenation + CO2 elimination)
• Collapsed alveoli more susceptible to lung infection
• Common post-op complication, prevent with strong pain control to enable clearing of mucous by coughing

Question 9

Interstitial lung disease has over 200 potential causes, what final pathway do they all share

Therefore what is its overall effect on gas exchange, compliance and elastic recoil?

Answer 9

• Thickening of the pulmonary interstitium, sometimes reversible sometimes not.
• Interstitium contains elastin, collagen fibres and fibroblasts.
• Impaired gas exchange (due to thickness), decreased compliance (as lungs are stiff) and increased recoil (due to increase in elastin)

Question 10

What are the potential causes of interstitial lung disease?

Answer 10

• Occupational - e.g.: asbestosis
• Treatment - e.g.: radiation, amiodarone
• Immunological - e.g.: sarcoidosis
• Idiopathic - idiopathic lung fibrosis accounts for 20% of cases

Question 11

What are the clinical symptoms and signs of interstitial lung disease

Answer 11

Symptoms:

• Dry cough
• Dyspnoea on exertion progressing to at rest
• Fatigue

Signs:

• Decreased lung excursion on palpation
• Inspiratory lung crackles
• Finger clubbing

Question 12

In Interstitial lung disease (diffuse pulmonary fibrosis) will FRC will reduced or increased & why?

Answer 12

Decreased, compliance reduced, elastic recoil increased.

Question 13

What is neonatal respiratory distress syndrome (NRDS) and who is at highest risk?

What are the typical signs?

Answer 13

• Babies born with insufficient surfactant, massively increased surface tension, reduced compliance and impaired gas exchange.
• Babies born before 30 weeks (surfactant produced at weeks 24-28, sufficient amounts by week 35)
• Grunting, nasal flaring, intercostal retractions, tachypnoea + cyanosis

Question 14

What is the effect of NRDS on the lungs, compliance and elastic recoil?

Answer 14

• Stiff lungs
• Decreased compliance
• Increased elastic recoil

Question 15

Will the FRC be increased or reduced in emphysematous COPD?

What would a compliance curve look like in emphysematous lungs + fibrotic lungs compared to healthy lungs?

Answer 15

• FRC will be increased, as elastic recoil is reduced
• Emphysematous lungs will have line that is raised and to the left (i.e.: increased compliance) due to reduced elastic recoil
• Fibrotic lungs will have line depressed and to the right (i.e.: decreased compliance) due to stiffened lungs and reduced compliance.

Question 16

Describe the pathophysiological basis for pneumothorax

Answer 16

• Small amount of air in pleural space keeps visceral and parietal pleura sealed.
• Chest wall or lung breached, i.e.: by stab wound, allows air to flow from atmosphere (higher pressure) –> pleural cavity (lower pressure)
• Ne negative intrapleural pressure = no intrapleaural seal, lung collapses due to inherent elastic recoil.

Question 17

What is hypoventilation?

What are some potential causes?

Answer 17

• Failure to breathe rapidly enough (low RR) or deeply enough (low tidal volume)
• Opiate OD, myasthenia gravis, DMD, pneumothorax, NRDS, severe acute asthma etc.