Session 2

Question 1

What is ventilation?

Answer 1

Ventilation is the process of inspiration and expiration The physical action of breathing and moving air into and out of the lung.

Question 2

What is quiet inspiration and expiration?

Answer 2

Normal resting breathing

• Volume of air being moved = tidal volume
• Breathing is a rhythmic and involuntary process
• Neurones in respiratory centre of brain automatically generate impulses to inspiratory muscles. we can also overide this for controlled breathing.

Question 3

Describe the lung mechanics of quiet inspiration and expiration

Answer 3

Inspiration

Air is drawn into the airways by active expansion of the thoracic cavity, which in turn expands the lungs. Volume and pressure have inverse relationship by where as volume increaes, pressure drops and this is what causes air to be drawn into the lungs, driven by this pressure difference. Intrapulmonary pressure drops below atmospheric pressure. Active process as muscles contaract to raise chest wall and flatten diaphragm. External intercostal muscles and diphragm contract in order to do this.

Expiration

Air expelled from the airways passively, by relaxing muscles used in inspiration. This reduces volume of thoracic cavity which reduces volume of lungs so intra-pulmonary pressure increases forcing air out of the lungs. Elastin in the lungs also help the lungs decrease in volume.

Question 4

What “keeps” the lungs against the chest wall?

Answer 4

• Lungs have a natural elastic recoil (like an elastic band)
• Tendency to want to “collapse in” especially with increased stretch
• Yet lungs are kept against chest wall without ‘physical’ attachment during inspiration and expiration…
• Pleural fluid found between visceral and parietal pleura (in intrapleural ‘space’) forms seal between lung and thoracic wall so lungs expand with the thoracic cavity

This is called the pleual seal: Surface tension between the pleural surfaces created by the presence of thin film of pleural fluid holds outer surface of lung to inner surface of chest wall.

Question 5

What happens between inspiration and expiration?

Answer 5

The Resting Expiratory Level (i.e. the state of equilibrium*) - the point before you inspire, having just expired…

• Lungs pull “in and up” due to lung elasticity
• Chest wall pulls “out” (its own elastic recoil) so opposite direction of force to lungs
• Diaphragm pulls “down” (due to passive stretch- not active contraction)
• Forces are equal and opposite so balance out (=no movement chest wall)
• Tendency to always want to return to this resting state (like an elastic band or spring)

Question 6

Which parts of breathing are active?

Answer 6

Inspiration (breathing in) is active

• Muscles contract to allow the chest wall and diaphragm to overcome inward pull of the lung recoil

Expiration (breathing out) is passive

• Muscles stop contracting
• Chest wall and diaphragm no longer overcome inward pull of lung recoil
• Return to resting expiratory level

Question 7

Describe the pressure existing between the pleura

Answer 7

The Inward Pull of the Lung Results in a Negative Pressure Between Pleura

• ‘Space’ between pleura = intrapleural space
• Pressure in this space is negative (relative to atmospheric pressure) due to elastic recoil of lung pulling visceral pleura inward and chest wall pulling parietal pleura outward
• Intrapleural pressure is negative throughout expiration and inspiration (becomes more negative up until end of inspiration)

Question 8

What happens if the integrity of the pleural seal is broken?

Answer 8

Negative Pressure in Intrapleural Space Draws Air from Outside Chest Wall into Space, Collapsing the Lung. Pneumothorax

Question 9

Draw a spirometry reading and label all of the different aspects

Answer 9

Question 10

What is tidal volume

Answer 10

Tidal volume represents the volume of air entering and leaving the lungs in a single breath (during quiet inspiration and expiration)

Question 11

What happens during forced inspiration and expiration?

Answer 11

Used during exercise but also when diseases affect the lungs

• Requires involvement of more muscles
• Accessory muscles of inspiration: Sternocleidomastoid Scalene muscles Serratus anterior Pectoralis major
• Accessory muscles of expiration (no longer passive): Internal intercostals, Abdominal wall muscles

Question 12

Work of Breathing and Lung Compliance

Answer 12

• Most effort is used in stretching the lungs
• “Stretchiness” of lungs is known as compliance
• Higher the compliance the easier it is to stretch
• Compliance of lung is determined by: Elastic tissue in lung and Surface tension forces of fluid lining alveoli

Question 13

What lines the alveoli surface and what does it do?

Answer 13

Alveoli surface lined with fluid.

• Surface tension of fluid limits expansion of the alveoli which decreases compliance making it difficult for aveoli (and therefore lungs) to expand
• Surfactant (secreted by type II pneumocytes in lungs) counters this as it has detergent properties and so acts to disrupt interaction between fluid molecules on alveolus surface, reducing the surface tension.

Surfactant is more effective at disrupting surface tension when its molecules are closer together (i.e. around smaller alveoli) therefore in:

• Larger alveoli - surfactant molecules spread further apart so are less effective at disrupting the surface tension. The Surface tension increases as alveoli increase in size i.e. as lungs expand [hence forced inspiration harder than quiet inspiration]
• Smaller alveoli - Surfactant molecules closer together so are more effective at disrupting surface tension of fluid resulting in reduced surface tension
• Reducing surface tension in smaller alveoli prevents pressure rising (within the alveolus) as a result of the smaller volume. It lso prevents small alveoli collapsing into big alveoli

Law of Laplace: Pressure= 2 x surface tension / radius

Think of the lungs as a collection of alveolar bubbles, all connected together

But there are alveoli of differing sizes…

Surfactant allows different sized alveoli to have same pressure within them

Surfactant: ensures pressures in alveoli do not drop despite increase in size

• Due to surfactant, surface tension in larger alveoli >>smaller alveoli
• Thus, pressure inside the bigger alveoli stays high despite it being bigger
• i.e. pressure does not drop despite increased ‘volume’ of the alveolus, as the increased pull ‘inwards’ from the surface tension counters this
• If pressure remains high in bigger alveoli, keeps pressures equal to smaller alveoli and so prevents collapsing of small alveoli into big alveoli

Question 14

When does the body begin to produce lung surfactant?

Answer 14

Surfactant is absent from alveoli until fetus >25 weeks

Respiratory distress syndrome is a condition that can be seen in premature babies, due to lack of surfactant

Question 15

How are the lungs fully ventilated to allow for gaseous exchange?

Answer 15

Air moves through a series of airways to reach alveoli so needs to overcome resistance to flow

• Tubes of small diameter have higher resistance to flow
• Many airways in lung are small so their individual resistance is high

Parallel Arrangement of Small Airways Compensates for Increase in their Individual Resistance

• Over whole expanse of airways
• Numerous airways running in parallel
• Compensates for increase in their ‘individual’ resistance
• In normal lungs: Highest resistance is in upper respiratory tree (trachea and large bronchi) and lowest in smaller airways [except when these become compressed during forced expiration]

Even a small decrease in tube size causes dramatic increase in resistance making it diddcult to fully expire

Airway resistance to flow adds little to the work (effort) of breathing in healthy lungs…most effort is in overcoming elastic recoil of lungs

Question 16

Define elasticity and compliance. What determines each of those? What is the other factor in ventilation?

Answer 16

Elasticity = The ability of an object or material to resume its normal shape after being stretched or compressed

Compliance= The ease with which an elastic structure can be stretched-distensibility

• Lung elasticity – primarily determined by elastin in the elastic fibres in the connective tissue of the lungs, and surface tension of the film of fluid that lines the alveoli.
• Lung compliance – also related to lung elastic fibres and surface tension of alveoli –but an INVERSE relationship

Another factor in ventilation is airways resistance –determined by airway diameter and surface tension

More compliant regions have less elastic recoil

Question 17

What is functional residual capacity?

Answer 17

FRC = Functional residual capacity = the volume of air in the lungs at the end of a quiet expiration

• Depends on balance between lung elastic recoil (inwards) and chest wall elastic recoil (outwards)
• If inward lung elastic recoil high (e.g. lung fibrosis) – lower lung volume at rest
• If lung elastic recoil low (e.g. emphysema) greater lung volume at rest (hyper inflated)

Question 18

Structure of a bronchus compared to the structure of a bronchiole?

Answer 18

In small bronchus theres small islads of cartilage whereas n bronchioles there is none

In small bronchus there are glands in the submucosa but in bronchioles there are not

Bronchus is larger than a bronchiole.

Question 19

Bronchioles have no cartilage. How do they stay open in expiration?

Answer 19

• Due to radial traction (outward tugging action) of the surrounding alveolar walls on bronchioles
• Prevents collapse of bronchioles during expiration

Loss of alveoli makes bronchioles more suceptible to collapse.

Question 20

What is surfactant?

Answer 20

Surfactant:

Ø Lines alveoli

Ø Mix of phospholipids and lipoproteins

Ø Diminishes the surface tension of the water film that lines alveoli

Ø Thereby decreasing the tendency of alveoli to collapse and the work required to inflate them

Made by cuboidal type 2 pneumocytes.

Question 21

What is hypoventilation?

Answer 21

Inability to expand chest

Question 22

Define pneumothorax

Answer 22

Air in the pleural space with loss of pleural seal

• If the chest wall or the lung is breached, A communication is created between pleural space and atmosphere
• Air flows from atmosphere (higher pressure) à 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:

Treated by draining air from the pleural space

A chest drain (tube) is inserted into the pleural space

The air is drained using an underwater seal - this prevents fluid or air from entering the pleural cavity

Question 23

What is interstitial lung disease

Answer 23

–Thickening of the pulmonary interstitium –the common final pathway almost always results in lung fibrosis –sometimes reversible – sometimes NOT!

–Early detection/treatment key to preventing irreversible progression

Interstitium contains: elastin fibres, collagen fibres fibroblasts and matrix substance

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

• If the exposure or injury persists or if the repair process is imperfect, the lung may be permanently damaged with increased fibrotic interstitial tissue replacing the normal capillaries, alveoli, and healthy interstitium.
• Fibrous tissue in the interstitium - Lung compliance is reduced - Lungs are stiff; harder to expand - Elastic recoil of the lungs is increased - the resting lung volume is smaller than normal – but RATE of airflow not impaired
• ‘Restrictive’ type of ventilatory defect on spirometry

–Clinical Symptoms – Dry cough – Shortness of breath – Dyspnea on exertion – Fatigue – Typically gradual, insidious progression

Signs: decreased lung excursion on palpation, bi-basal end inspiratory lung crepitations, Finger clubbing, Pleural effusions

Gas exchange is also affected - ie not just air movement in an airway – also a diffusion problem In interstitial lung disease (diffuse lung fibrosis) alveolar capillary membrane is thickened - Increases diffusion distance

Controlled exercse is used as helpful treatment - not fully understood - thought to stretch lungs so increases compliance - strengthens ventilatory muscles - patients become more used to the shortness of breath and how to handle it.

Question 24

Respiratory distress in the new-born

Answer 24

Not enough lung surfactant in neonates making lung expansion difficult as the surface tension too high. In preterm babies (severe < 30 weeks)

Features of respiratory difficulty from birth

Ø grunting,

Ø nasal flaring,

Ø intercostal and subcostal retractions

Ø Rapid respiratory rate (tachypnea)

Ø cyanosis

Surfactant :

• Produced by Type II alveolar cells; starts at 24 –28 weeks gestation;
• increasing amounts by 32 weeks
• Usually sufficient by 35 –36 weeks

Preterm babies -< 37 weeks :

• Insufficient surfactant so 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 25

What can make quiet expiration difficult?

Answer 25

– ↑airways resistance: Asthma, Chronic obstructive pulmonary disease (COPD) – COPD c/w asthma also have destruction of elastic fibres, ↓elastic recoil of lungs –

Question 26

– Why are problems with airflow typically worse in expiration compared with inspiration?

Answer 26

Expiration is passive as pressure in the lungs has increased

Question 27

What is idiopathic pulmonary fibrosis and cryptogenic fibrosing alveolitis?

Answer 27

In approximately 20% of cases of interstitial lung disease aetiology unknown – called Cryptogenic fibrosing alveolitis (CFA) or idiopathic pulmonary fibrosis

Question 28

What is COPD?

Answer 28

Chronic Obstructive Lung Disease (COPD)

• Third leasing cause of death worldwide – worldwide prevalence ~10%
• Caused by smoking and/or inhaled pollutants interacting with genetic vulnerability
• Clinical syndrome characterised by chronic respiratory symptoms with associated pulmonary abnormalities – all conditions share impaired airflow that is not fully reversible – classic definition encompasses two medical conditions – Chronic bronchitis – Emphysema – Above two conditions actually co-exist in many people
• Pre-COPD - relatively new term – airflow impaired but no clinical symptoms yet and “normal spirometry” – but at very high risk for developing COPD in the next 5 years
• Even full fledged COPD typically underdiagnosed – considered disease of the older adult
• Should be recognised earlier! Earlier interventions normalise/slow lung function decline

Question 29

What is chronic bronchitis - airways disease?

Answer 29

• Chronic bronchitis is a disease of the airways– from bronchi to bronchioles
• Mucus hypersecretion (from goblet cells and sub mucus glands)
• Reduced cilia – mucus is not cleared effectively
• Effects of above lead to – airflow limitation/obstruction by luminal obstruction of small airways – epithelial remodeling, – alteration of airway surface tension predisposing to collapse
• Clinical diagnosis – cough productive sputum > three months of the year for > one year

Causes of excessive mucus in COPD:

Inflammatory cells, infection and oxidative stress cause increased production and poor ciliary clearence, airway occlusion and resp muscle weakness cause reduced removal.

Increased airways resistance –different mechanisms, but airway diameters compromised -all give obstructive pattern

Question 30

What is emphysema, how is it involved in COPD?

Answer 30

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

Ø Inflammatory cells accumulate; which release elastases and oxidants which destroy alveolar walls and elastin

Ø Protease mediated destruction of elastin is an important feature

Ø Reduced elasticity is a key problem – airway trapping

Ø Also, large air spaces result in reduced surface area for gas exchange

Barrel chest seen - flattened diaphragm and enlarged thoracic cavity - hyper inflated

Question 31

Compare emphysema and pulmonary fibrosis

Answer 31

Emphysema

• Loss of elastic tissue
• Increased compliance and reduced elastic recoil
• Hyper inflated: Barrel chest
• Small airways collapse in expiration (loss of radial traction)
• Air trapping (Obstruction and ↓recoil)
• Obstructive pattern on spirometry testing

Pulmonary Fibrosis

• Increase of fibrous tissue
• Less compliant Stiff - harder to expand
• Smaller lungs
• Decreased functional residual capacity and other lung volumes
• No airway obstruction
• Restrictive disease on Spirometry testing

Question 32

What is atelectasis?

Answer 32

Atelectasis (lung collapse)

Inadequate expansion of air spaces

• In new-born babies: failure of alveoli to expand at birth (e.g. lack of surfactant)
• Compression collapse: due to – air in pleural cavity (pneumothorax) – fluid in the pleural cavity (pleural effusion)
• Compression from abdominal distension – Compresses alveoli
• Resorption collapse: due to obstruction – Airway obstructed; air downstream of blockage slowly absorbed into blood stream – Alveoli collapse
• Collapse due to obstruction of a large airway (eg Lung cancer, mucus plugs)

Question 33

What is a cough?

Answer 33

Cough is an explosive expiration of air from the lungs

• Cough reflex is co-ordinated by cough center in the medulla oblongata
• initiated by irritation of mechano- and/or chemoreceptors in the respiratory epithelium. Normal cough involves the following steps:
• Deep inspiration
• The glottis is closed by vocal cord adduction
• Strong contraction of the expiratory muscles (abdominal muscles, internal intercostal muscles) which builds up intrapulmonary pressure
• Sudden opening of the glottis causes an explosive discharge of air.

Question 34

What is dead space? Relation to tidal volume?

Total Pulmonary ventilation

Alveolar ventilation

Answer 34

Anatomical dead space = The volume of air in the conducting airways

Alveolar dead space = air in alveoli which do not take part in gas exchange (These are alveoli which are not perfused or are damaged)

Physiological dead space = Anatomical dead space + Alveolar dead space.

Tidal volume = Anatomical Dead space + alveolar ventilation

Total Pulmonary ventilation (Minute volume)= Tidal volume x respiratory rate

Alveolar ventilation = (Tidal volume – Dead space) x respiratory rate