2

Question 1

What is the definition of ventilation?

Answer 1

• process of inspiration and expiration
• physical action of breathing and moving air in and out of the lungs
• ventilation does not equal respiration

Question 2

What is “quiet” inspiration and expiration? What is the volume of air called?

Answer 2

• Volume of air being moved= tidal volume
• Breathing is a rhythmic and involuntary process
• neurones in the respiratory centre of brain automatically generate impulses to inspiratory muscles

Question 3

Describe and explain the lung mechanics in quiet inspiration

Answer 3

• air is drawn into the airways by ACTIVE expansion of the thoracic cavity, which in turn expands the lungs
• just before you take a breath in, the pressure equates to atmospheric pressure
• when you breathe: pressure drops below atmospheric pressure
• changes in volume changes the pressure which allows air to go in and out
• STILL EXPENDING ENERGY DURING QUIET INSPIRATION
• diaphragm is flattened (>70%)
• external intercostal muscles also contract
• helps to increase the intrathoracic volume
• as volume goes UP pressure goes DOWN

Question 4

Describe the increase/decrease in lung volume during normal respiration (I.e. reserve volume)

Answer 4

• lung volume is not maximal
• it can be increased to the extent of the INSPIRATORY RESERVE VOLUME (IRV)
• can also breathe out more than the rest, by using the EXPIRATORY RESERVE VOLUME (ERV)
• cannot however empty our lungs completely, so even after forced expiration a residual volume (RV) will remain

Question 5

Describe the significance of lung capacities

Answer 5

• while lung volumes change with changes in tidal volume, lung capacities DO NOT
• defined relative to fixed points in the breathing cycle: maximum inspiration, maximum expiration, and the end of a quiet expiration
• inspiration capacity: from end of quiet expiration to max inspiration (inspiratory reserve + tidal volumes)
• functional residual capacity: volume of air in the lungs at the end of a quiet expiration
• vital capacity: inspiration capacity + expiratory reserve
• total lung volume: vital capacity + reserve volume

Question 6

Describe and explain the lung mechanics in quiet expiration

Answer 6

• air is expelled from airways PASSIVELY by relaxing muscles used in inspiration
• reduces volume of thoracic cavity
• reduces volume of lungs
• NO expenditure of energy, just muscles relaxing
• pressure rises higher than atmospheric pressure and volume decreases which forces air out of the lungs
• is passive due to elastic recoil; no muscles used

Question 7

What is the anatomical dead space?

Answer 7

• the volume of the conducting airways
• only part of tidal volume is used for gas exchange, the rest fills the conducting airways
• conducting airways extends from nostrils to and including the bronchioles

Question 8

What is the alveolar dead space?

Answer 8

• air in alveoli which are not perfused, are damaged, or do not take part in gas exchange
• ventilation of these alveoli are wasted

Question 9

What is the physiological dead space?

Answer 9

Physiological dead space= anatomical dead space + alveolar dead space

Question 10

What “keeps” the lungs against the chest wall?

Answer 10

• lungs are like rubber band and have a natural elastic recoil
• pleural seal keeps the lungs against the chest wall

Question 11

What is the pleural seal?

Answer 11

• pleural fluid found between visceral and parietal pleura (in intrapleural space) forms seal between lung and thoracic wall
• allows lungs to expand with thoracic cavity
• 10-15ml fluid between the two layers creates surface tension which allows a seal to form
• ensures the chest wall and lungs move together
• seal also allows structures to smoothly slide over each other as well

Question 12

Explain the resting expiratory level

Answer 12

• the bit in between quiet inspiration and quiet expiration
• the state of equilibrium: the point before you inspire, having just expired
• have two forces acting against each other
• inward: lung’s elasticity pulls “in and up”, and surface tensions generates an inwardly directed force that favours lung volumes
• outward: chest wall pulls “out” (has own elastic recoil), at rest this elasticity favours outward movement of the chest wall
• diaphragm pulls “down” (due to passive stretch -not active contraction)
• net effect: forces are equal and opposing so creates a balance, creates a NEGATIVE PRESSURE within intrapleural space (no movement in chest wall)
• tendency to always return to this resting state

Question 13

Explain how ventilation disturbs the equilibrium

Answer 13

• inspiration is active: muscles contract to allow the chest wall and diaphragm to overcome inward pull of the lung recoil
• expiration is passive: muscles stop contracting, chest wall and diaphragm no longer overcome inward pull of lung recoil, returning to resting expiratory level

Question 14

Describe the intrapleural space

Answer 14

• the space between the pleura
• pressure in this space is NEGATIVE (relative to atmospheric pressure) due to: elastic recoil 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)
• returns to resting (negative) pressure at the end of quiet expiration

Question 15

What happens when the integrity of the pleural seal is broken

Answer 15

• negative pressure in intrapleural space draws air (with atmospheric pressure) from outside chest wall into space, collapsing the lung
• pneumothorax (air in chest) can occur

Question 16

What is forced inspiration and expiration?

Answer 16

• going beyond quiet inspiration and expiration
• forced inspiration: when ventilation is increased as in exercise or resistance to respiration is present
• accessory muscles are used: SCM, scalene muscles, serratus anterior, pectoralis major
• kids often experience forced inspiration
• forced expiration: also used during exercise or when disease affects the lungs (no longer passive)
• accessory muscles are used: internal intercostal muscles, abd wall muscles (external and internal obliques and rectus abdominus muscles)

Question 17

Why is energy expended during inspiration?

Answer 17

• to stretch the lungs

- to overcome airway resistance

Question 18

What is compliance?

Answer 18

• the stretchiness of lungs
• defined as the volume change per unit pressure change
• most effort is used in stretching the lungs
• higher the compliance the easier it is to stretch

Question 19

What determines the compliance of the lungs?

Answer 19

• elastic tissue in the lungs

- surface tension forces of the fluid lining alveoli

Question 20

Explain how surface tension affects alveoli

Answer 20

• alveoli are lined with film of fluid which has to be stretched as lungs expands
• increase in ares is opposed by the surface tension of the lining fluid b/c gas-liquid interface always tends towards achieving the minimum surface area
• surface tension of flood limits expansion of alveoli
• decreases compliance making it difficult for alveoli to expand

Question 21

Explain the significance of surfactant

Answer 21

• secreted by type 2 pneumocytes
• has detergent properties and is a mixture of phospholipids and proteins
• hydrophilic ends lie in the alveolar fluid with the hydrophobic ends projecting into the alveolar gas
• without we could not create enough pull to counteract the elastic tension
• acts to disrupt interaction between fluid molecules on alveolus surface…reducing surface tension

Question 22

Why is surfactant more effective at disrupting surface tension when its molecules are closer together?

Answer 22

• large alveoli means the surfactant molecules spread further apart making them less efficient
• less effective at disrupting the surface tension
• as alveoli increase in size (when lungs expand) the surface tension increases
• but smaller alveoli means the surfactant molecules are closer together, which increases their concentration on the surface and acts more efficiently to reduce the surface tension
• more effective at disrupting surface tension of fluid and reduced surface tension
• force required to expand smaller alveoli is therefore less than that required to expand large ones

Question 23

How does surfactant stabilize the lungs?

Answer 23

• alveoli comes in varying shapes and sizes
• if surface tension was same in all, smaller alveoli would have higher pressure in it
• if two unequal sized alveoli were connected by an airway the smaller alveolus with a higher pressure will empty into the larger alveolus which has a lower pressure
• big bubbles eat the small bubble
• surfactant prevents the small alveoli collapsing into big alveoli
• in big alveoli, surfactant molecules are spread further apart making them less efficient so it increases the surface tension
• as a result different sized alveoli can have the same pressure within them stabilizing the lungs

Question 24

When does surfactant first appear in a human?

Answer 24

-when fetus is greater than 25 weeks

Question 25

What is respiratory distress syndrome? (Neonatal respiratory distress syndrome)

Answer 25

- condition that can be seen in premature babies, due to lack of surfactant - results in stiffer lungs - deficiency of surfactant in premature babies, particularly those less than 30 weeks old - features of respiratory difficulty from birth: grunting, nasal flaring, intercostal and subcostal retractions, tachypnea, cyanosis - Without surfactant the surface tension in the fluid lining the alveoli is high - This makes the lungs harder to expand at birth; lung expansion is incomplete; some alveoli remain collapsed (airless); no gas exchange occurs in these alveoli - The lung is stiffer and harder to expand –lung compliance is low -Increased effort is required to breathe  Results in impaired ventilatio - Typically, babies have signs of respiratory distress (cyanosis, grunting, intercostal and subcostal recession). - The treatment of RDS includes surfactant replacement via an endotracheal tube, and supportive treatment with oxygen and assisted ventilation

Question 26

What is Poiseulle’s Law?

Answer 26

- tubes of small diameter have higher resistance to flow - many airways in lungs are small - individual resistance is high (smaller the tube, higher the resistance to flow) - resistance of a single tube increases sharply with falling radius - but the combined resistance of the small airways is normally low b/c they are connected in parallel over a branching structure where the total resistance to flow in the smaller branches is lower than a larger branch - reason why there are many branches in the lungs: combined resistance to air flow is smaller than one large air tube) - higher resistance in the upper respiratory tract

Question 27

Why is it harder to forcibly breathe out?

Answer 27

- squashing down narrow airways and resistance is really high - collapses airways without cartilage, even a small decrease in tube size causes dramatic increase in resistance

Question 28

What is the relationship between compliance and elastic recoil?

Answer 28

- compliance is a measure of how stretchy the lung is (measure of distensibility) - elastance is a measure of elastic recoil= the tendency to return to their original size when stretched - as compliance goes up, elasticity goes down and vice versa

Question 29

Compare the structure of a bronchus to a bronchiole

Answer 29

- bronchus: robust and stiff, has small islands of cartilage and glands in submucosa - bronchiole: has no cartilage and no glands

Question 30

How are bronchioles kept open?

Answer 30

- alveoli are attached to the bronchiole which keep it open even as pressure goes up in expiration - due to radial traction (outward tugging)

Question 31

What percentage of pneumocytes does the alveoli have?

Answer 31

- 90% type 1 pneumocytes | - 10% type 2 pneumocytes

Question 32

Explain interstitial lung disease

Answer 32

- thickening of the pulmonary interstitial which can be caused by a variety of diseases - almost always leads to lung fibrosis - early detection/treatment is key to prevention - pulmonary interstitum: space between the alveolar epithelium and capillary endothelium crucial for gas exchange - interstitum contains: elastin fibres, collagen fibres, fibroblasts and matrix substance - The lungs are stiffer and harder to expand, since collagen fibres are less stretchy than elastin fibres, so lung compliance is reduced. - The elastic recoil of the lungs is increased. (Note: the term elastic recoil is not limited to the recoil of elastin fibres, but by the tendency of BOTH elastin and collagen fibres to return to their original size when stretched). - The lungs are smaller than normal, due to the increased elastic recoil (see cartoon) - It causes a 'restrictive' type of ventilatory defect, - On examination, chest expansion is reduced - Thickening of alveolar walls increases the distance oxygen has to diffuse from alveolar air to the blood (and vice versa for CO2). - The effect on diffusion of oxygen is much greater than that on CO2 which is more soluble than oxygen - Symptoms: shortness of breath, reduced exercise tolerance, dry cough - Signs include tachypnoea (increased respiratory rate), tachycardia, reduced chest movement (bilaterally), and coarse crackles. - common causes: asbestos, coal-miners disease, drugs, mouldy hay, autoimmune-mediated inflammation, unknown injury (20% not treatable), methotrexate - signs: deceased lung excursion on palpation, bi-basal end inspiratory lung drepitations, finger clubbing, pleural effusions

Question 33

Explain COPD

Answer 33

- caused by smoking and/or inhaled pollutants interacting with genetic vulnerability - usually two medical conditions: chronic bronchitis and emphysema

Question 34

Explain chronic bronchitis

Answer 34

- disease of the airways: from bronchi to bronchioles - mucus hypersecretion (from goblet cells and sub mucus glands) - reduced cilia so mucus is not cleared effectively (colliery-mucus escalators not working properly) - mucus plugging causes increased airway resistance - airflow limitation by luminal obstruction of small airways - epithelial remodeling - alteration of airway surface tension predisposing to collapse

Question 35

Why is airway obstruction worse in expiration than inspiration?

Answer 35

- negative pressure in the pleural space during inspiration helps to keep the lower airways open - positive intrapulmonary pressure during expiration exacerbates narrowing of intrathoracic airways

Question 36

Explain emphysema

Answer 36

- air sacs disease - loss of elastin and breakdown of alveolar walls causing increased lung compliance and narrowing of small airways (non-reversible) - pt’s have barrel chest because lungs are hyper-inflated and diaphragm flattened - The lungs are easier to expand as there is less elastin; they are more stretchy i.e. The lung compliance is increased - The elastic recoil of the lungs is reduced - At rest the lungs are hyper-inflated, (i.e. more expanded than normal), due to the loss of elastic recoil - The small airways are narrowed due to the loss of elastic fibres exerting an outward pull (radial traction) on the small bronchioles - Airway narrowing causes an 'obstructive’ type of ventilatory defect on Spirometry. - Symptoms: shortness of breath, reduced exercise tolerance

Question 37

Explain pneumothorax

Answer 37

- occurs when chest walls or the lungs is breached - communication is created between pleural space and atmosphere - air flows from atmosphere (high pressure) into the pleural cavity (lower pressure) - until the pleural pressure = atmospheric pressure - pleural seal is lost - lung elastic recoil not counter-balanced by negative pleural pressure - lung collapses to unstretched size - treatment: draining air from the pleural space, chest drain (tube) is inserted into the pleural space - air is drained using an underwater seal which prevents fluid or air from entering the pleural cavity

Question 38

Explain asthma

Answer 38

- chronic inflammatory process which may be triggered by allergic/non-allergic stimuli - inflammation causes airway narrowing due to bronchial smooth muscle contraction, thickening of airway walls by mucosal oedema and excess mucus production which can partially block the lumen

Question 39

Explain atelectasis

Answer 39

- aka lung collapse - inadequate expansion of air spaces - in new-born babies: failure of alveoli to expand at birth (ex. Lack of surfactant) - compression collapse: due to air in pleural cavity (pneumothorax), fluid in the pleural activity (pleural effusion) - compression from abd distension which compresses the alveoli - resorption collapse: due to obstruction of airways, air downstream of blockage slowly absorbed into bloodstream and alveoli collapse - resorption collapse: collapse due to obstruction of a large airway (ex. Lung cancer, mucus plugs)

Question 40

Explain hypoventilation

Answer 40

-due to poor expansion of the thoracic cavity or lungs -caused by respiratory muscle weakness or severe thoracic wall deformities -very stiff lungs or severe airway obstruction can cause poor ventilation of the lungs -injuries causing hypoventilation -brain stem: opiates, head injury -spinal cord: trauma -phrenic and intercostal nerves: Gillian-Barre syndrome -neuromuscular junction: myasthenia gravis -muscles of respiration: inherited muscle disease (duchenne muscular dystrophy) Chest wall: severe obesity -pleural cavity: pneumothorax, large pleura effusions -poor lung compliance (stiff lungs): NRSD -upper airway obstruction: laryngeal oedema, foreign body -high airway resistance: very severe acute asthma