gas exchange in lungs Flashcards
Why is pressure used rather than concentraion when quantifying gases?
2 main reasons?
This is because gases react, dissolve, and diffuse more in accordance with their pressure than concentration.
This is because pressure takes into account other factors that affect the properties/behaviour of a gas, such as temperature.
what is partial pressure?
partial pressure describes the degree to which an individual gas in a mixture of gases contribute to total pressure
total partial pressure calculation
what do you take into account?
ππππ‘ππ = π(π»2 π) + βπ(πΆπππ π‘ππ‘π’πππ‘ πππ ππ )
partial pressure of individual gas
What do you take into account?
How do you calculate it?
ππππ = (ππππππππ‘πππ β π(π»2 π)) Γ π_πππ
Partial pressures for gas phases can be calculated by subtracting water vapour pressure (which also contributes to total pressure and varies from 0kPa in dry air to approximately 6kPa in fully warmed, humidified air within the lung) from the total pressure (atmospheric) , and then multiplying the resulting value by the individual gasβ mole fraction
(the fraction of total moles represented by the individual gas, e.g. oxygen at sea level = 0.21 or 21%).
water vapour pressure
contributes to total pressure and varies from 0kPa in dry air to approximately 6kPa in fully warmed, humidified air within the lung
what is PO2 in alveolar (humidified) air at sea level, if PBarometric = 100kPa?
(100 - 6) x 0.21 = 19.74
What happens if barometric pressure decreases (e.g. altitude)
Less total/atmospheric pressure but same mole fraction of o2 hence less o2 in the air
What determines how much gas dissolves in a liquid?
equation?
what does the partial pressure of gas dissolved in a liquid reflect?
The concentration of a gas dissolved within a liquid is determined by the partial pressure and solubility of the gas:
πΆππππππ‘πππ‘πππ=ππππ‘πππ ππππ π π’ππ Γππππ’πππππ‘π¦
The partial pressure of gas dissolved in a liquid reflects the amount of gas that would dissolve (at equilibrium) if the liquid was placed in contact with a gas phase of equivalent partial pressure.
why canβt partial pressures for different gases in liquid be compared?
comparisons cannot be made between different gases (e.g. oxygen and carbon dioxide) as the solubility will vary.
co2 solubility - 5.0 mL.L-1.kPa-1
if PaCO2 = 5.0 kPa, the concentration of CO2 dissolved in the plasma will be
carbon dioxide has a water solubility of approximately 5.0 mL.L-1.kPa-1.
This means there will be 5.0 mL of CO2 per litre of blood for each kPa of pressure.
Therefore, if PaCO2 = 5.0 kPa, the concentration of CO2 dissolved in the plasma will be:
[CO2] = 5.0 mL.L-1.kPa-1 x 5 kPa = 25 mL
properties of alveoli to allow good gas exchange to occur
3 factors
a large surface area (both individually and cumulatively),
thin outer structure (typically one cell thick),
richly innervated by capillaries
structures and mediums blood gases need to bypass
what is the jounrey of o2 to transporter?
1) O2 enters the alveolar airspace from the atmosphere.
2) O2 dissolves in ALF. (alveolar lining fluid)
3) O2 diffuses through alveolar epithelium, basement membrane, & capillary endothelial cells.
4) O2 dissolves in blood plasma
5) O2 binds Hb molecule
any kind of change in these structures like depth or consistency will affect rate
why must diffusion be rapid to allow adequeate oxygenation of blood?
how long does it take for rbc to pass capillary in tyoical conditions?
how does this chnage during exercise?
In typical conditions, it takes approximately 0.75 seconds for a red blood cell to pass through a pulmonary capillary, during which time oxygenation must occur.
During intensive exercise, where pulmonary blood flow is increased, this time may even decrease to as little as 0.25 seconds - not an issue with healthy individuals
consequence of thickening of blood gas barrier and further problems during exercise
reduce diffuision rate hence the rate of gas exchnage + rate at which o2 is oxygenated so by 3/4 secs, full oxidation doesnβt take place
problem is further worsened when blood flow is increased -> during exercise, CO increaes and rbc flow through pulmonary capillaries at increased speed hence takes 0.25s than 0.75s to flow through which means a lot less diffusion takes place
rate of diffusion equation for gas exchange
equation?
π ππ‘π ππ πππππ’π πππβ(ππ’πππππ ππππ)/γπ·ππ π‘ππππγ^2 Γ (π_π΄ β π_πΆ)
The rate of diffusion (on which gas exchange depends) is determined by the partial pressure gradient between the two areas, the size of the diffusion distance, and the surface area.
defects in partial pressure gradient
pathology and problems with it?
hypoventilation (type II respiratory failure)
donβt breathe in a sufficient rate to bring fresh air into body + cope with demands
therefore decreased pressure gradient
defects in surface area
pathology?
emphysema will reduce SA
defects in distance hence barrier thickness
2 pathology?
Fibrosis = β basement membrane thickness (scarring)
Pulmonary oedema (e.g. pneumonia) = β thickness of fluid layer/oedema
The role of ventilation in determining the level of gas exchange
what is changed and what for?
changing the rate of alveolar ventilation (the volume of fresh air reaching alveoli per unit of time), in order to modulate the partial pressure gradients between the alveoli and blood
to meet the o2/co2 demands of the body
ventilation/perfusion ratio
why does this need to be matched?
Blood flow through pulmonary capillaries (perfusion, πΜ) needs to be matched to alveolar ventilation (πΜ_π΄) to enable efficient gas exchange, as there is a maximum amount of O2 each unit of blood can carry.
v/q ratios
patholgies of over and under 1?
v/q cause
>1 hypoperfusion (βdead space effectβ)
=1 normal
<1 hypoventilation (βshuntβ)
How is v/q mismatch reduced?
what maintains ventilation-perfusion coupling?
how does it do this? detector and effect?
what is the net effect?
Ventilation-perfusion coupling is maintained by hypoxic vasoconstriction which diverts blood flow from poor to well ventilated alveoli
the way it does this is that within the wall of endothelium, there are receptors that can detect or respond to level of o2, relatively when it becomes hypoxic (less o2)
in response to less o2, the smooth muscle in the wall of the capillary contracts and vasoconstricts hence it is harder for blood to flow through (increased R)
as it is harder for blood to flow through that vessel, blood is diverted to a different vessel that isnβt constricted and this is because, this new vessel hasnβt been exposed to hypoxia so wonβt be constricted
the net effetc is that blood is diverted from hypoxic alveoli to well ventilated alveoli therefore help match ventilation to perfusion (VQ coupling)
how does v/q ineqality affect co2 and o2?
In theory, V-Q inequality affects both O2 and CO2 exchange, however in most cases, βPaCO2 will induce a reflex hyperventilation that clears the excess CO2 (but doesnβt βPaO2) because of v:q mismatch)
v/q mismatch doesnt refer to chnages in overall level of ventilation or perfusion to the lungs
not necessarily referring to changes in the overall level of ventilation or perfusion to the lungs, but rather situations where V/Q ratios vary substantially between alveolar units
Dead-space effect (ventilation without perfusion)
what will the ratio look like? effect?
why can this occur? What are the affected regions of the lungs referred to as?
If perfusion is reduced relative to ventilation, V/Q ratio will increase (V/Q >1) and the inspired oxygen will in effect be βwastedβ and not participate in gas exchange.
This can occur due to reduced blood supply to specific regions of the lung (e.g. pulmonary embolism, damage/blockade of blood vessels). The affected regions of the lung are referred to as βphysiologic dead-spaceβ as they are effectively not participating in gas exchange, despite the presence of O2, similar to the anatomic dead-space consisting of the airways).
Dead-space effect (ventilation without perfusion)
e.g pulmonary embolism ( v/q = > 1)
effect of embolism? v/q value? what happens to other regions and why?
overall effect of the lungs with pulomonary emobolism?
in theory how can this be compensated for? effect if not?
what happens in practice? why might this not happen?
embolism occludes pulmonary artery supplying a region in the lung. underperfused alveoli will have high V/Q as blood canβt flow to that region hence less perfusion. Therefore, the opposite will happen in other alveolis as blood is diverted there as the CO is the same hence V same but Q up so V:Q ratio is less.
In the case of a pulmonary embolism (a block of an artery in the lungs), the overall perfusion of the lungs as a whole may not decrease if blood is simply diverted through other pulmonary arteries/capillaries.
In theory, increased ventilation of these areas of the lungs may compensate for the reduction in gas exchange in others. Otherwise, hypoxaemia and hypercapnia (increased PaCO2) will occur.
In practice, any increase in PaCO2 will rapidly result in an increase in ventilation due to chemoreceptor reflexes (unless airways are obstructed or respiratory effort reduced due to disease), reducing PaCO2 back to normal levels.
reaons for dead space effect
3 reasons?
Reduced perfusion of lung regions, causes an increase in πΜ/πΜ ratio:
Heart failure (cardiac arrest) Blocked vessels (pulmonary embolism) Loss/damage to capillaries (emphysema)
The affected alveoli = physiological dead-space, as no/reduced gas exchange occurs.
pulmonary shunt
reason for this?
what happens?
Reduced ventilation of alveoli or limits to diffusion cause a decrease in πΜ/πΜ ratio:
Cardiac shunts
Pneumonia, acute lung injury, respiratory distress syndrome, atelectasis (cut off part of lungs)
Blood from the right heart to the left, without taking part in gas exchange (shunt).
When does pulmonary shunt occur?
conditions when extent of shunt is limited?
what has a greater severity of pulmonary shunt?
While ventilation to particular regions of the lung can be reduced in obstructive airway diseases such as asthma and COPD, the extent of shunt that occurs in these conditions is relatively limited.
In contrast, cardiac shunts, pneumonia, acute lung injury, RDS and atelectasis and all associated with a greater severity of pulmonary shunt.
How does shunt respond to o2 therapy?
how does hypoxaemia caused by shunt respond to o2 therapy?
why is this the case?
why canβt well ventilated areas compensate with o2 therapy?
what is the overall effect?
Hypoxaemia caused by shunt is associated with a much more limited response to supplemental oxygen therapy than that associated with other V/Q inequalities.
This is because regardless of degree of oxygenation occurring in blood perfusing well-ventilated alveoli, it will eventually mix with deoxygenated blood returning from areas affected by shunt, reducing the overall PaO2
The vast majority (>98%) of oxygen carried in blood is transported bound to haemoglobin. As saturation of haemoglobin is typically >95% at physiological oxygen pressures, administering supplemental oxygen cannot increase oxygen saturation in well-ventilated regions of the lung sufficiently to compensate for the deoxygenated blood with which it will eventually mix.
o2 from well ventilated alveoli can not compensate from o2 you lose from other alveoli. hence blood will come from venous system to poor functional alveoli and doesnβt get oxygenated at all and the overall effect is hypoaemic as overal level of o2 decreases in systemic circulation
