Alveolar Gases & Diffusion Flashcards
what is the difference between Pa and PA?
Pa – partial pressure in arterial blood
PA – Partial pressure in alveoli
what is the PIo2 and PIco2 at the mouth?
Inspired Oxygen partial pressure (PIo2) = 20 kPa
Inspired CO2 partial pressure (PIco2) = 0 kPa
in the conducting zone, what are the changes in Po2 + Pco2 during inspiration?
There are changes in Po2 + Pco2 as we are breathing in/out tidally
Inspiration (I):
When we breathe in the conducting zone fills with fresh air.
Therefore, the conducting therefore has the same levels of gas tensions as the air/mouth:
Po2 = 20 kPa
Pco2 = 0 kPa
in the conducting zone, what are the changes in Po2 + Pco2 during expiration?
Expiration (E):
When breathe out, conducting zone fills with expired air from alveoli
Therefore, the conducting zone now has different levels of gas tension than air/mouth.
Po2 = 13 kPa (↓ as oxygen has been extracted)
Pco2 = 5 kPa (↑)
However, there is no gas exchange occurring in the conducting zone so this has no effect on the gas tensions in the blood.
how many litres is the alveolar space?
what is the gas tension like in the AS? include values
Alveolar Space = 2.5L
Despite tidal breathing gas tension is the alveolar space is stable (does not change)
Po2 = 13 kPa
Pco2 = 5 kPa
state the 2 reasons why gas tension is the alveolar space is stable
It does not change for two reasons:
We add very little air into this space (~350ml of air mixes into the 2500 ml) with each breath, (we are not emptying and filling alveolar space each time like in the conducting zone)
Movement of air into alveoli is only via diffusion (due to large SA)
does blood in the pulmonary capillaries have high levels of gases?
Blood coming into the pulmonary capillaries is from rest of body, therefore it has low levels of gases.
what are the partial pressures of venous O2 and CO2?
why is this the case?
Mixed venous gas tensions:
Partial pressure of venous oxygen (PVo2) = 5 kPa
Partial pressure of venous carbon dioxide (PVco2) = 6 kPa
As blood passes through the lungs, it equilibrates across the alveolar capillary membranes - blood leaving the lungs has same gas tensions as alveolar gases.
what happens to arterial gas tensions (include values)?
Stable Arterial Gas Tensions:
Pao2 = 13 kPa again
Paco2 = 5 kPa again
Therefore, in normal conditions, Pco2 and Po2 in blood leaving the lungs is set by the alveolar partial pressures of these gases.
Alveolar partial pressure set by other factors (another flashcard)
I.e. alveolar partial pressures sets blood gas tensions
By altering alveolar gas tensions –> alter blood gas tensions
What determines alveolar Pco2 tensions?
Metabolic Rate: ↑ metabolism –> ↑ CO2 production (V.CO2) - will concentrate alveolar CO2 (PAco2)
More CO2 coming into lungs, will diffuse into alveoli and raise this value
Alveolar Ventilation: ↑ in alveolar ventilation (V.A) will dilute alveolar CO2 (PAco2)
BUT, PACO2 remains constant BC as we are breathing more so we blow out CO2 out of the alveoli faster than it arrives
Therefore, alveolar CO2 is:
proportional to CO2 production
inversely proportional to alveolar ventilation
Combining the two: Therefore, alveolar CO2 is proportional to CO2 production / alveolar ventilation
what is this equation used for?
Use equation in photo to calculate what would happen to alveolar CO2 if we change alveolar ventilation and/or metabolic rate.
The equation above for PAco2 defines a metabolic hyperbol as it defines the relationship between alveolar CO2 and alveolar ventilation at any particular metabolic rate (V.CO2).
what does this graph show?
Solid Black line: Metabolic rate = 250ml/min (basal metabolic rate)
Normally we have an alveolar CO2 of 5 kPa because normal alveolar ventilation is around 5 L. min-1
If we hyperventilate (ventilating alveolar gases more than metabolic needs), the alveolar CO2 will fall to the level of inspired CO2 (tends to 0 kPa)
If we hypoventilate (ventilating alveolar gas less than metabolic needs), PCO2 rises steeply
Aim of breathing is to set a ventilation rate for a set metabolism to keep alveolar CO2 at 5 kPa which then allows for arterial CO2 to be 5 kPa
what does this graph show?
Dotted Red line: Exercise –> ↑ in metabolic rate (V.CO2) to 500 ml.min-1
Curve shifts upwards, therefore at any level of alveolar ventilation, alveolar CO2 will be higher.
Doubling metabolic rate (not changing ventilation), doubles alveolar CO2
But when we exercise, we do increase our ventilation:
Ventilation (V.A) increases in direct proportion with metabolic rate (V.CO2)
This allows us to hold alveolar CO2 constant (remains constant at 5 kPa)
what are the clinical uses of arterial CO2?
Arterial CO2 (Paco2) (a measure of alveolar CO2) is a clinical measure of the adequacy of alveolar ventilation
If Arterial CO2 is higher than expected, person is not breathing enough
The definition of hypoventilation and hyperventilation based on whether arterial CO2 is too high or too low.
What determines alveolar Po2 tensions?
Exactly same as for PAco2 => Metabolic Rate and Alveolar Ventilation
Both have Hyperbolic curves though the O2 is in a different direction because ↑ ventilation causes ↑ oxygen in alveoli.
Also inspired Po2 is not zero like it is for inspired Pco2 (taken in account in equation below)
Therefore, we can derive the following equations
If metabolic rate ↑ –> ↑V.O2 (nothing else changes), (subtraction becomes greater) - PAo2 ↓
If alveolar ventilation ↑ (+ nothing else changes), (subtraction becomes less) - ↑ PAo2
what happens when you combine the CO2 and O2 equations and alveolar gas equations?
clinical relevance?
As R is a constant (0.8) if alveolar CO2 ↑ alveolar O2 ↓
Clinically relevant: if we don’t breathe enough, alveolar CO2 ↑ –> alveolar O2 ↓
Can be solved by utilising higher PIo2 in order to ↑ alveolar O2 to a higher level
what is the important clinical use of alveolar gas equation?
Calculating PAO2
PaCO2 which is easily obtained from an arterial blood sample, can replace PACO2 in the above equation as there is no measurable difference between these 2 values
PIo2 is easily determined and taken as its value when dry at 37oC
Must remove water vapour pressure (PH2O)(6.26Kpa), at 37oC, from total pressure (PB) then multiply it by fraction of oxygen in the air.
PIo2 = (PB – PH20) x (% oxygen) - Plug PIo2 into alveolar gas equation.
R (essentially RQ) will be 0.8 unless diet is unusual
This then provided us will all values to calculate PAO2 (only unknown value in equation!)
describe the movement of respiratory gases across the lung
what are the 3 layers?
Respiratory gases need to diffuse through a gaseous (air) phase and a liquid phase (interstitial fluid + into cells) in order to move across alveolar-capillary membrane.
Alveolar-capillary membrane made up of 3 thin layers (short distance):
1. Alveolar epithelium - lining of alveolus
2. Basal lamina
3. Capillary endothelium
Oxygen diffuses from alveolus into plasma of the capillary along its partial pressure gradient and CO2 moves from the capillary plasma into the alveolus along its partial pressure gradient.
what is Graham’s Law?
(Diffusion of a gas through a gas)
Graham’s Law: Diffusion in gaseous phase is dependent upon ΔP and is ∝ to 1 / √MW (bigger molecules diffuse slower than small ones)
ΔP = partial pressure difference
MW = molecular weight
Molecular weight of CO2 is greater than O2
∴ CO2 (larger molecule) diffuses slightly slower (0.85x as fast) in gas than O2
what is Henry’s Law?
CO2 and O2 have different solubility coefficients (α)
conc of gas = partial pressure x solubility coefficient
Therefore CO2 diffuses across a liquid gradient 23x faster for the same partial pressure.
what is diffusibility of CO2 or O2 calculated as?
Gases need to diffuse through gases AND liquids - combine Graham’s and Henry’s Laws:
Diffusibility of CO2 or O2 is calculated as:
[Diffusibility ratio in air] x [diffusibility ratio is liquid]
0.85 x 23 = 20 - CO2 diffuses 20 times more easily than O2 across alveolar – capillary membrane (if same partial pressure difference across the membrane)
However, we Do NOT have same partial pressure difference across alveolar-capillary membrane
PAo2 = 13 kPa vs PVo2 = 5 kPa –> Partial pressure difference = 8kPa
PAco2 = 5 kPa vs PVo2 = 6 kPa –> Partial pressure difference = 1kPa
However despite a much smaller alveolar-capillary difference (1 vs. 8 kPa), still more CO2 can be transferred per minute than O2 (due to its higher diffusibility)
Therefore, any diffusion limitations (Membrane thickens or Liquid forming on alveolar side (instead of air)) will show up firstly as problems with O2 rather than CO2 transfer.
Therefore, we will observe hypoxia before hypercapnia (a person will be low in O2 before they become high in CO2)
what does this graph show?
X axis: shows the time blood will spend within a pulmonary capillary during one transit
Typically at rest = 0.75 second
Y-axis: partial pressure of gas in blood
Assume alveolar partial pressure of all 3 gases is always 13 kPa (this is that of oxygen)
what is the effect of time and health on pulmonary capillary Po2?
Same graph as before, but just for oxygen
This shows a very high diffusion reserve for oxygen:
There is still lots of time left (2/3 of transit time) after equilibration has occurred (PA = Ppc)
This means if we ↑ speed of blood through lungs and ↓ transit time in pulmonary capillary we will still have full equilibration
Therefore we can ↑ cardiac output while exercising to allow more oxygen to get around body, while the blood still being equilibrated (13 kPa of O2)
describe why results would be abnormal and severely abnormal on the graph?
Abnormal on graph: patient only just reaches equilibration within the transit time - very little diffusion reserve
Therefore during exercise (transit time ↓) the patient’s blood will not reach an equilibrated state - hypoxic, breathlessness
Severely abnormal on graph: not reach equilibration in transit time - breathless even at rest.
They are diffusion limited, as diffusion barrier is too great for time we have for equilibration.
what would happen to a normal persons at altitude and what are the consequences?
Normal person at altitude:
At a higher altitude there is a lower partial pressure of oxygen in the atmosphere.
This means there is a lower partial pressure of oxygen in the alveoli
The means there is a decrease in the partial pressure gradient (PP still 5kpa in venous blood but no longer 13kpa in alveoli)
This will ↓ rate at which oxygen moves across alveolar-capillary membrane
This will look like the abnormal line on the graph (equilibration occurs towards the end of transit time)
Consequences at high altitude: edge of diffusion limitation –> exercise at altitude –> hypoxic.
what is pulmonary diffusing capacity?
Pulmonary diffusing capacity: Ability to diffuse gases from alveoli to capillary
Blue box = alveolar-capillary membrane in the lungs
P1 = Alveolar partial pressure of a gas
P2 = Pulmonary capillary partial pressure of that same gas
what is flow of gas (V.) across diffusion barrier proportional to?
Flow of gas (V.) across diffusion barrier is proportional to:
Diffusibility of gas (d) (in air and liquid)
Area (A) (greater the area the greater the flow)
1/T thickness (inversely proportional) (the greater the thicker of the barrier the less diffusion occurs)
Pressure gradient (P1 – P2)
Therefore, you get equation:
what does this graph show about body mass?
Graph: Body mass of different animals plotted against lung diffusing capacity of each animal
Log scale - gradient of 1 - therefore ↑ in body mass results in ↑ diffusing capacity/
There is a strong correlation between mass of animal, diffusing capacity and maximal O2 consumption
So, our maximal oxygen consumption is limited by our diffusive capacity which is linked to our body mass.
How to measure pulmonary diffusing capacity?
calculate flow of gas (V.)
In the lungs the area and thickness is difficult to measure.
Therefore d, A and T are combined to give - diffusion constant, DL - Diffusing capacity
Therefore, through rearranging you get:
DL (diffusing capcity) = flow of gas / pressure difference
how do you measure pulmonary diffusing capacity (DL)?
Difficult to measure an individual’s DL directly for O2 because Po2 changes along pulmonary capillary (between 5 – 13 kPa) so there is no fixed value to represent P2
Therefore, we measure DL using carbon monoxide instead.
This is because CO as a high affinity for haemoglobin –> no effect on partial pressure in pulmonary capillary (unlike O2) makes P2 effectively zero
NB: CO is toxic so use low conc. 0.3% for a single breath
So P1 = is the small amount of CO we use in the alveolar space (PAco)
P2 = 0 as all molecules of CO are bound to haemoglobin so have no effect on the partial pressure in pulmonary capillary
So P1 – P2 = P1 = PACO
V.CO is measured by amount of CO we put in and the amount that comes out again.
So, by plugging all the values in we can measure diffusing capacity of the lung for CO
So by plugging in the acquired values we get 175 ml of CO passing across a normal lung per minute per KPa of CO
To convert this to the diffusing capacity of the lung for O2 we use the conversion factor (1.25) (takes into account different weights of molecules)
what factors cause an increase in diffusion path length (T)?
↑ diffusion path length (T) (green box shows thickening)
↑ diffusion path length will reduce DL
Increased diffusion path length may occur due to:
Thickened alveolar-capillary membrane (e.g. due to fibrosis)
Accumulation of lung fluid (pulmonary edema)
Increased intracapillary distance
E.g. anaemia (low haemoglobin) - reduces diffusion, as ↓ ability of binding oxygen)
Tests of DL cannot distinguish between A + T, as the two are combined in the equation
Use history + other tests to distinguish to see if A or T is the cause.
