mechanics of breathing

Question 1

Q: However why is the fall in alveolar pressure large enough to be observed?

I.e. why any differences in pressure between the alveoli and atmosphere not instantly negated by the movement of air?

Answer 1

There is a delay due to the time taken for air to move.

As air passes through airways, it generates resistance as it comes into contact with the airway surface

Impaired airway function = Insufficient ventilation

Question 2

ohm’s law

what is the equation?

Answer 2

𝐴𝑖𝑟𝑓𝑙𝑜𝑤 (𝑉) “=” (Δ𝑃𝑟𝑒𝑠𝑠𝑢𝑟𝑒 (𝑃))/(𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 (𝑅))

↑ΔP = ↑airflow ↑resistance = ↓airflow

Question 3

poiseuille law
equation?
factor that determine the level of resistance?

Answer 3

𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 (𝑅) “∝ “ 1/〖𝑟𝑎𝑑𝑖𝑢𝑠〗^4

As an airway’s radius decreases, the resistance increases (and the airflow decreases) dramatically
(small change in radius, big change in resistance)

Question 4

why can increased resistance reducing airflow, not be overcome by increased pressure alone?

2 reasons?

Answer 4

this has specific physical limitations, e.g. the effort/force required to do so may not be able to be generated, or the airway might be completely obstructed.

Question 5

what can decrease airway lumen (hence increase resistance)

4 different reasons
effect of all 4 things

Answer 5

Contraction of airway smooth muscle, excessive mucus secretion, oedema/swelling of the airway tissue, damage to the integrity of the airways structure (i.e. loss of patency)

will all reduce the size of the airway lumen, increasing airway resistance and decreasing airflow

Question 6

what other than decreased airway lumen can increase resistance?

Answer 6

pattern of airflow

Where airflow changes from a linear to a turbulent pattern, increased airway resistance is generated

Question 7

How is turbulent airflow achieved
2 reasons
which type of airflow pattern is not efficient?

Answer 7

Turbulence occurs where high velocities of airflow are achieved (e.g. during forced breathing manoeuvres) or if there is a sudden decrease in luminal area such as in obstructed airways

air flows in a multi-directional manner and is not efficient

Question 8

what is responsible for the wheezing sound in patients with obstructed airways?

Answer 8

The vibration generated by the turbulent airflow is responsible for the wheezing sound produced in patients with obstructed airways

Question 9

what is laminar flow?

Answer 9

airflow in a linear manner in a single plane - the norm

Question 10

what is airway patency?

Answer 10

patency refers to the state of being open or unobstructed; a ‘loss of patency’ = closing/obstruction

Question 11

what maintains airway patency/keeps open?

where is the majority of airways positioned?

Answer 11

maintained by elastic fibres within the wall of the airway and radial traction

majority of airways are positioned within surrounding lung tissue which has elastic properties - the airways are pulled open by their connections to the surrounding tissue

Question 12

How does the elastic fibres helps with airway patency?

what happens during inspiration?
what happens during expiration? why can we notice airway obstruction during expiration?

Answer 12

As the lungs expand during inspiration, the lung tissue and airways contained within are stretched upon.

During expiration, the lung tissue and airways are compressed. This process helps to explain why airway obstruction is often more noticeable during expiration.

structural integrity of the airways is sufficient to prevent collapse

Question 13

how can airway patency be reduced during forced expiration?

what happens to intrapleural pressure during forced expiration? effect of this?

why is this not an issue for healthy indivduals?
who is it an issue for?

Answer 13

pressure differentials between the intrapleural space and airways can reduce airway patency during forced expirations.

When intrapleural pressure becomes positive (as can occur during forced expiration), collapsing force will be exerted onto the airways.

In healthy individuals, the structural integrity of the airways is sufficient to prevent collapse,

however in diseases involving impaired airway structure (e.g. COPD), this can be problematic

Question 14

loss of airway patency e.g copd

why does airways flatten during expiration? what is degraded?
what is particularly problematic in copd? what twso thimgs are reduced and why? effect of this?

Answer 14

occurs due to degradation of airway structure elastin hence becomes rigid and can’t cope with the level of compression that occurs during expiration therefore it flattens

Decreased structural integrity of the airways to maintain airway patency during forced expiration is particularly problematic in COPD, as the simultaneous loss of elastic recoil within the lung tissue means that both radial traction of the airways and lung recoil and reduced. The later means that greater force is required to compress the lungs during expiration, however the more force that is exerted to maintain ventilation and airflow, the more obstructed the patient’s airways will become

Question 15

loss of airway patency vs constriction

Answer 15

loss of aireay patency is different to constrcition, narrowing and as the whole thing just flattens hence collapses shut

Question 16

what is lung compliance?

what pressure change is looked at in the relationship?

Answer 16

Lung compliance quantifies the relationship between the level of expansive force applied to the lung and the resulting change in lung volume

This relationship between the change in lung volume produced by a particular changed in transpulmonary pressure is termed ‘lung compliance’, and essentially describes how easily the lungs can be distended

Question 17

what is transpulonary pressure?

difference between which 2 pressures and what does it determine?

how is it calculated?

Answer 17

The difference between the pressure within the alveoli and intrapleural space (termed ‘transpulmonary pressure’) determines the level of force acting to expand or compress the lungs.

Transpulmonary pressure is calculated by subtracting intrapleural pressure from alveolar pressure
(Ptp = Palv – Pip), and describes the force
acting to expand (if Ptp > 0) or
compress (if Pt < 0) the lungs

Question 18

inspiration and intrapleural pressure

what happens to intrapleural pressure and why?

Answer 18

During inspiration, increasing levels of negative intrapleural pressure are generated as lung volume increases due to the elastic properties of lung tissue (similar to the way an elastic band generates greater recoiling force the more it is stretched).

Question 19

How does compliance effect lung volume?

high vs low compliance?

Answer 19

Higher lung compliance = less elastic recoil = less force required to inflate = ↑ volume change per pressure change (↑gradient on volume-pressure curve)

Lower compliance = more elastic recoil = more force required to inflate = ↓volume change per pressure change (↓ gradient on volume-pressure curve)

Question 20

How is lung compliance calculated?

equation?

Answer 20

Lung compliance is calculated by dividing a change in lung volume by the associated change in transpulmonary pressure

𝐶𝑜𝑚𝑝𝑙𝑖𝑎𝑛𝑐𝑒 (𝐶l)=Δ𝑉𝑜𝑙𝑢𝑚𝑒/Δ𝑃𝑟𝑒𝑠𝑠𝑢𝑟𝑒

Question 21

compliance graph

gradient of the curve on v/p graph -> which is a greater level of compliance?

Answer 21

Compliance is expressed as the gradient of the curve.
Steeper curve = Greater level of lung compliance

‘Looser’/easier to inflate lung = greater lung compliance

Stiffer/harder to inflate lung = lower lung compliance

Question 22

how to measure static and dynamic compliance?

which point is used to measure compliance?

Answer 22

For static compliance (measurements taken whilst airflow =0), the steepest part of the curve is used,

for dynamic compliance (measurements taken in the presence of airflow), the gradient between the end tidal inspiratory and end tidal expiratory points is used:

Question 23

what factors + diseases affect lung compliance?

3 factors and the associated disease related to it?

Answer 23

chest wall mechanics - scoliosis muscular dystrophy + obesity (decrease)

alveolar surface tension - neonatal respiratory distress syndrome (Decrease)

elastin fibres - fibrosis (decrease) and COPD (increase)

Question 24

scoliosis muscular dystrophy + obesity - lung compliance

why does it reduce lung compliance?

Answer 24

scoliosis in obesity makes it harder for lungs to expand due to the fact that there’es excess weight on the person’s trunk (needs to be overcome when lungs expand)

Question 25

pulmonary fibrosis - lung compliance

effect on compliance and why?

Answer 25

deposition of collagen due to firbrosis
leads to scarring of the lungs + thick tissue being deposited
less compliance

Question 26

copd - compliance

effect on compliance and why?

Answer 26

degradation of lungs hence loss of elastin fibres means more compliant
it is easier to expand lungs but bad for recoil which can lead to lung collapse

Question 27

copd + fibrosis in lung compliance graph

why?

Answer 27

copd/emphysema higher and to the left

fibrosis lower and to the right

Question 28

why is a bubble formed in alveolis?

what are alveoli lined with? why?
what creates a bubble?

Answer 28

Alveoli are lined with fluid to enable gas exchange (the gas molecules dissolve into water before diffusing.

The water-air interface formed between the lining fluid and pseudo-spherical alveolar airspace essentially creates a bubble

Question 29

why does surface tension arise?

effect of surface tension?

Answer 29

Within the bubble, surface tension arises due to the relative strength of hydrogen bonds between water molecules combining to exert an overall collapsing force toward the centre of the bubble.

Question 30

why is surface tension bad?

Answer 30

H-bonds create a collpasing force towards the centre
The collapsing force produced at the water-fluid interface generates pressure

hence to expand the alveoli, you need to overcome this force

Question 31

How to calculate the pressure within a specific bubble?

equation?
equation if T remains constant?
hence effect of smaller the alveoli?

Answer 31

Law of Laplace
𝑃 =2𝑇/𝑟 (T = surface tension and r = radius of bubble)

Therefore if T remains constant:
𝑃 ∝1/𝑟
(The smaller the alveoli, the larger the pressure generated)

Question 32

What would happen if 2 bubbles of different radius were connected to each other (e.g. different size alveoli connected via airways)?

Answer 32

Pressure and bubble radius are inversely proportional (pressure increases as radius decreases), which means that smaller bubbles generate greater pressure than larger ones.

As gases naturally move from areas of high to low pressure, if bubbles of varying size are connected (such as different size alveoli connect by airways), the smaller bubble will empty into larger ones due the pressure gradient.

Question 33

Within the lungs, the pressure gradients that would be created between different sized alveoli would result in smaller alveoli collapsing into larger ones. This would thus make inflation of the lung very difficult

How is this overcome?

Answer 33

the presence of pulmonary surfactant, a phospholipoprotein secreted by type II pneumocytes (alveolar cells).

Question 34

what is surfactant?

Answer 34

Surfactant molecules are amphipathic, with hydrophilic head and hydrophobic tail regions, and so will naturally position themselves at the air-liquid interface.

Question 35

How does surfactant reduce surface tension?

Answer 35

The presence of the surfactant molecules then acts to disrupt the attractive forces between water molecules (H bonds), reducing surfacing tension hence less collapsing pressure generated.

Question 36

How does surfactant act to equalise pressure and volume across varying alveoli?

what happens to surfactant as alveolar size increases? effect of this?
what is the net effect of this to equalise pressure?

Answer 36

As alveolar size increases during inflation, the concentration of surfactant molecules at the interface decreases (as upon inflation there will be the same number of surfactant molecules within an increased surface area hence the local conc of surfactant will decrease, less impact on surface tension, more compressive force).

The net effect is that where pulmonary surfactant is present, surface tension (and thus pressure generated) increases with increasing alveolar surface area.

This means that air will naturally flow from larger (more inflated) alveoli to smaller ones, helping to distribute air across the lung during inspiration

Question 37

How does Pulmonary surfactant helps to prevent alveolar oedema?

effect of surface tension on hydrostatic pressure? effect of this? effect of surfactant?

Answer 37

The surface tension produced at the air-liquid interface also reduces hydrostatics pressure in the alveolar tissue.

This acts to pull fluid out of the surrounding pulmonary capillaries and into the alveoli and interstitial tissue.

By reducing surface tension, pulmonary surfactant helps to prevent alveolar oedema due to excessive fluid being pulled from capillaries

Question 38

What is neonatal respiratory distress sydrome?

occurs in who? what is the condition?

Answer 38

Neonatal respiratory distress syndrome (NRDS) is a condition that occurs in infants born prematurely, and who develop and produce insufficient levels of pulmonary surfactant (surfactant production at week 24-28).

Question 39

problems with nrds

3 main effects?
what can be damaged from all of this?

Answer 39

This deficiency results in respiratory failure due to the alveoli collapsing, decreasing lung compliance (‘stiffer’ lungs), and alveolar oedema reducing gas exchange.

The increased forces and pressures involved within the lung also damage alveoli and innervating capillaries.

Question 40

treatment for nrds

2 different treatments?
who is at higher risk and why?

Answer 40

NRDS is treated by either supplementation of affected infants with artificial surfactant, and/or by administering glucocorticoids (which increase surfactant production via maturation of type 2 pneumocytes) to mothers deemed high risk (e.g. mothers with poor diabetic control – insulin appears to affect pneumocyte maturation - or those at risk of premature birth).

Question 41

summary of nrds

who is at risk?
what happens?
effect of this?
net effect of this?

Answer 41

Premature birth, maternal diabetes, congenital developmental issues
↓
Insufficient surfactant production
↓
Stiff (low compliance) lungs, alveolar collapse, oedema
↓
Respiratory failure
↓
Hypoxia
↓
Pulmonary vasoconstriction, endothelial damage, acidosis, pulmonary + cerebral haemorrhage.

Question 42

When ex vivo lungs are inflated with saline (rather than air), how does compliance change?

Answer 42

In classic experiments, physiologists compared compliance in ex vivo lungs inflated with air vs. lungs inflated with saline.

Saline-filled lungs required less pressure to inflate (↑ compliance).

Washing lungs with saline before inflating with air, produced lungs that required more pressure to inflate (↓ compliance).