mechanics of breathing Flashcards
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?
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
ohmβs law
what is the equation?
π΄ππππππ€ (π) β=β (Ξππππ π π’ππ (π))/(π ππ ππ π‘ππππ (π ))
βΞP = βairflow βresistance = βairflow
poiseuille law
equation?
factor that determine the level of resistance?
π ππ ππ π‘ππππ (π ) ββ β 1/γπππππ’π γ^4
As an airwayβs radius decreases, the resistance increases (and the airflow decreases) dramatically
(small change in radius, big change in resistance)
why can increased resistance reducing airflow, not be overcome by increased pressure alone?
2 reasons?
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.
what can decrease airway lumen (hence increase resistance)
4 different reasons
effect of all 4 things
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
what other than decreased airway lumen can increase resistance?
pattern of airflow
Where airflow changes from a linear to a turbulent pattern, increased airway resistance is generated
How is turbulent airflow achieved
2 reasons
which type of airflow pattern is not efficient?
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
what is responsible for the wheezing sound in patients with obstructed airways?
The vibration generated by the turbulent airflow is responsible for the wheezing sound produced in patients with obstructed airways
what is laminar flow?
airflow in a linear manner in a single plane - the norm
what is airway patency?
patency refers to the state of being open or unobstructed; a βloss of patencyβ = closing/obstruction
what maintains airway patency/keeps open?
where is the majority of airways positioned?
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
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?
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
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?
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
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?
occurs due to degradation of airway structure elastin hence becomes rigid and canβt 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 patientβs airways will become
loss of airway patency vs constriction
loss of aireay patency is different to constrcition, narrowing and as the whole thing just flattens hence collapses shut
what is lung compliance?
what pressure change is looked at in the relationship?
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 βlung complianceβ, and essentially describes how easily the lungs can be distended
what is transpulonary pressure?
difference between which 2 pressures and what does it determine?
how is it calculated?
The difference between the pressure within the alveoli and intrapleural space (termed βtranspulmonary pressureβ) 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 β Pip), and describes the force
acting to expand (if Ptp > 0) or
compress (if Pt < 0) the lungs
inspiration and intrapleural pressure
what happens to intrapleural pressure and why?
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).
How does compliance effect lung volume?
high vs low compliance?
Higher lung compliance = less elastic recoil = less force required to inflate = β volume change per pressure change (βgradient on volume-pressure curve)
Lower compliance = more elastic recoil = more force required to inflate = βvolume change per pressure change (β gradient on volume-pressure curve)
How is lung compliance calculated?
equation?
Lung compliance is calculated by dividing a change in lung volume by the associated change in transpulmonary pressure
πΆπππππππππ (πΆl)=Ξππππ’ππ/Ξππππ π π’ππ
compliance graph
gradient of the curve on v/p graph -> which is a greater level of compliance?
Compliance is expressed as the gradient of the curve.
Steeper curve = Greater level of lung compliance
βLooserβ/easier to inflate lung = greater lung compliance
Stiffer/harder to inflate lung = lower lung compliance
how to measure static and dynamic compliance?
which point is used to measure compliance?
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:
what factors + diseases affect lung compliance?
3 factors and the associated disease related to it?
chest wall mechanics - scoliosis muscular dystrophy + obesity (decrease)
alveolar surface tension - neonatal respiratory distress syndrome (Decrease)
elastin fibres - fibrosis (decrease) and COPD (increase)
scoliosis muscular dystrophy + obesity - lung compliance
why does it reduce lung compliance?
scoliosis in obesity makes it harder for lungs to expand due to the fact that thereβes excess weight on the personβs trunk (needs to be overcome when lungs expand)
pulmonary fibrosis - lung compliance
effect on compliance and why?
deposition of collagen due to firbrosis
leads to scarring of the lungs + thick tissue being deposited
less compliance
copd - compliance
effect on compliance and why?
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
copd + fibrosis in lung compliance graph
why?
copd/emphysema higher and to the left
fibrosis lower and to the right
why is a bubble formed in alveolis?
what are alveoli lined with? why?
what creates a bubble?
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
why does surface tension arise?
effect of surface tension?
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.
why is surface tension bad?
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
How to calculate the pressure within a specific bubble?
equation?
equation if T remains constant?
hence effect of smaller the alveoli?
Law of Laplace
π =2π/π (T = surface tension and r = radius of bubble)
Therefore if T remains constant:
π β1/π
(The smaller the alveoli, the larger the pressure generated)
What would happen if 2 bubbles of different radius were connected to each other (e.g. different size alveoli connected via airways)?
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.
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?
the presence of pulmonary surfactant, a phospholipoprotein secreted by type II pneumocytes (alveolar cells).
what is surfactant?
Surfactant molecules are amphipathic, with hydrophilic head and hydrophobic tail regions, and so will naturally position themselves at the air-liquid interface.
How does surfactant reduce surface tension?
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.
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?
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
How does Pulmonary surfactant helps to prevent alveolar oedema?
effect of surface tension on hydrostatic pressure? effect of this? effect of surfactant?
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
What is neonatal respiratory distress sydrome?
occurs in who? what is the condition?
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).
problems with nrds
3 main effects?
what can be damaged from all of this?
This deficiency results in respiratory failure due to the alveoli collapsing, decreasing lung compliance (βstifferβ lungs), and alveolar oedema reducing gas exchange.
The increased forces and pressures involved within the lung also damage alveoli and innervating capillaries.
treatment for nrds
2 different treatments?
who is at higher risk and why?
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 β insulin appears to affect pneumocyte maturation - or those at risk of premature birth).
summary of nrds
who is at risk?
what happens?
effect of this?
net effect of this?
Premature birth, maternal diabetes, congenital developmental issues
β
Insufficient surfactant production
β
Stiff (low compliance) lungs, alveolar collapse, oedema
β
Respiratory failure
β
Hypoxia
β
Pulmonary vasoconstriction, endothelial damage, acidosis, pulmonary + cerebral haemorrhage.
When ex vivo lungs are inflated with saline (rather than air), how does compliance change?
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 (β compliance).
Washing lungs with saline before inflating with air, produced lungs that required more pressure to inflate (β compliance).
