Ventilation & Perfusion Flashcards

1
Q

is there a difference between alveolar and arterial partial pressure of oxygen?

A

There is a difference between alveolar and arterial partial pressure of oxygen
NB. due to high diffusibility of CO2 we do not generally see A-a difference in Pco2
Alveolar oxygen partial pressure = ~13 kPa
This is set and maintained by combination of: metabolism (oxygen removed) and ventilation (oxygen added)
Aim of ventilation is to provide sufficient oxygen to match metabolism to keep PaO2 = 13.

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2
Q

explain the pathway of the flow of blood between the heart and lungs?

A
  1. Venous blood returns to the heart with a partial pressure of oxygen ~5 kPa
  2. This blood passes into the pulmonary capillary where it equilibrates, as diffusion occurs
  3. The partial pressure of oxygen at end of capillary therefore becomes the same as alveolar pressure (13 kPa)
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3
Q

Why is Po2 of blood leaving the aorta less than Po2 in alveolus? (i.e. What causes an A-a difference?)

A

Normal alveolar-arterial Po2 difference is 1 kPa
There are two main reasons why PAo2 ≠ Pao2
1. Shunts
2. Ventilation-Perfusion (V/Q) Mismatch

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4
Q

explain what shunt is

A

This is when blood moves from the right side of the heart to the left side, without becoming oxygenated (I.e. blood has bypassed oxygenating system)
We all have a small amount of this blood

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5
Q

explain what ventilation-perfusion (V/Q) mismatch is?

A

This is when the amount of ventilation of the lungs is not matched precisely by blood flow (perfusion) through the lungs:
Lung at rest receive:
~4 litres/min of alveolar ventilation (V.)
5 litres/min blood flow (Q.)
Total lung ventilation / perfusion ratio: V / Q = 0.8
Therefore, we do not quite have same amount of ventilation as we do blood flow
This slight difference causes small ↓ in arterial Po2
NB: V. and Q. are not evenly distributed throughout the lung

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6
Q

what do both shunts and ventialation-perfusion mismatch do?

A

Shunts & V/Q mismatch both contribute equally to small Po2 A-a difference normally observed in healthy individuals
Anything that ↑ shunt fraction and/or V/Q mismatch will ↑ the A-a difference
This will be expressed as falls in PaO2 (hypoxia)
NB: A-a difference ↑ gradually with age (as the V/Q ratio changes). The difference is around 2.3 kPa at 60 years (Calculated: Age/30 + 0.3 kPa)

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7
Q

what do Right-Left (R-L) shunts do?

A

R-L natural shunts contribute about ½ of the Po2 A-a difference in health
Most venous blood passes though the ventilated regions of lung, becoming oxygenated.
However, some venous blood does not and is R-L ‘shunted’ 🡪 ‘wasted perfusion’
Moves from right to left side of heart without becoming oxygenated
Adding unoxygenated venous blood to arterial blood is called ‘venous admixture’
When R-L shunting occurs 🡪 V/Q mismatch 🡪 V/Q closer to 0

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8
Q

what do natural R-L shunts do?
what are 2 examples?

A

Normally only 1-2% of cardiac output is R-L Shunted.
This has little effect on function.
Examples of Natural R-L Shunts:
- Thebesian Veins (venae cordis minimae)
- Bronchial Circulation

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9
Q

what do Thebesian veins do?

A

Thebesian Veins (venae cordis minimae): numerous, small valveless venous channels that open directly into the chambers of the heart from the capillary bed in the cardiac wall
They contain arterial blood that originally has gone to supply the cardiac tissue itself, but instead of then draining into venous system it drains directly into left ventricle (form of venous admixture)
This a form of collateral circulation unique to heart

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10
Q

what happens during bronchial circulation?

A

Bronchial circulation arises from thoracic aorta
70% of total bronchial blood flow supplies the intrapulmonary bronchi/bronchioles
Bronchial blood is only ~1% of pulmonary arterial blood flow
Deoxygenated blood then passes through bronchopulmonary veins and joins the pulmonary vein to drain into left atrium
Therefore, this blood from the lungs does not drain into venous system (+ go around rest of body).

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11
Q

what do pathological R-L shunts cause?
example?

A

Any ↑ in the degree of shunt will ↑ the A-a difference and lead to ↑ in deoxygenation of arterial blood 🡪 symptoms of breathlessness
EXAMPLE: Pulmonary disease:
Anything that blocks the Airways (e.g. foreign object or mucus) will prevent airflow downstream of block
A Collapsed bronchi/alveoli will also prevent air flowing into this area
If blood flows to this area of the lung that does not receive ventilation we get a R-L shunt.
R-L shunt 🡪 V/Q will fall from normal 0.8 towards 0 (which would be a total shunt)

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12
Q

what are cardiovascular anatomical abnormalities (shunts)?
when do they occur?

A

Cardiovascular anatomical abnormalities often occur in neonates
They include Atrial and/or ventricular septal defects.
You get a L-R shunts (NOT R-L shunts) because of the way the ‘holes in heart’ allow blood to pass from the higher pressure left atrium/ventricle to lower pressure right side of the heart
I.e. Oxygenated blood passes in to deoxygenated areas.
Problems occur due to ↑ load which right heart is not designed to take but now has to bear
↑ load leads to pulmonary problems which then cause congestion 🡪 impact back on to left heart
Treated with surgery.

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13
Q

explain 3 examples of cardiovascular anatomical abnormalities

A
  1. Patent ductus arteriosus: in the foetus, blood flow to the lungs is prevented by ductus arteriosus, which allows blood to move from the R heart into aorta without entering the higher resistance lungs
    In birth this should shut, but in some individuals it does not
  2. Atrial septal defect: septum between left and right atria is not completely closed, therefore blood flows from the higher-pressure L heart into lower pressure R heart.
  3. Ventricular septal defect: septum between ventricles not completely closed so blood flows from the higher-pressure L heart into lower pressure R heart.
    Both septal defects put a load onto the right heart that is not normally expected, causing the problems stated above.
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14
Q

why is there variation in the ventilation an perfusion of diff parts of the lung?

A

V/Q mismatch is around 0.8 for the whole lung.
But there is variation in both ventilation and perfusion in different regions of the lung.
The main cause for variation in ventilation is gravity and compliance:
Both gravity and compliance cause variations in the distribution of pleural pressure
The varied distribution of pleural pressure then causes variations in ventilation

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15
Q

think of question

A

Schematic:
At FRC, there is a greater retraction of the lung from chest wall at apex than at the base.
This is because the mass of the lung and the effect of gravity causes:
The apex of the lung to pull away from the chest wall (greater retraction)
The base of the lung to push towards the chest wall/diaphragm (retraction is less)
Greater retraction causes a greater negativity of pleural pressure.
Therefore, there is a greater negative intrapleural pressure at the apex than at the base:
At apex: Greater retraction 🡪 Greater negative Ppl of -1 kPa
At base: less retraction 🡪 less negative Ppl of -0.25 kPa

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16
Q

what does the graph show?

A

Greater negative intrapleural pressure results in greater distention:
Base of the lung (-0.25 kPa): relatively inflated
Apex of the lung(-1 kPa): More inflated (due to greater retraction giving greater negative intrapleural pressure 🡪 greater volume)
THIS IS AT FRC
Therefore, at FRC the lung units from apex to base are NOT equally inflated.
This means the Apex alveoli are far more inflated than alveoli at base

17
Q

Why does this lead to greater ventilation at base of lung than apex?

A

EXAMPLE: Ppl needs to fall (become more negative) by 0.3 kPa for FRC to ↑ by 1 L
Therefore -0.25 kPa at base will fall to -0.55 kPa and -1 kPa at apex will fall to -1.3 kPa
(these falls in intrapleural pressure shown by black horizontal lines on graph below)
How will this affect volumes of air entering the apex and base?
Base: located on steep part of compliance curve
Therefore a ↓ in intrapleural pressure, leads to significant ↑ in lung volume (show by red vertical line) (shown by greater increase in lung volume)
Greater change in volume => greater ventilation
Apex: located on flat part of compliance curve
At the apex the Alveoli are reaching their elastic limit and so cannot inflate much more.
Therefore, for the same change in pleural pressure, there is a smaller increase in lung volume (so smaller ventilation)
Therefore, greater ventilation occurs in base of the lung rather than the apex
Therefore, total resting alveolar ventilation (V.A) of 4 litres/min is distributed unequally through the lungs 🡪 the base receiving 2.5 x more ventilation than the apex
I.e. When you take a breath in, more air goes to base of lung (greater airflow) than to apex
NB: this is a continuum across the lung so middle region of lung receives more air than apex as well

18
Q

describe the distribution of perfusion (blood flow) through the lung

A

Now we are looking at distribution of perfusion (not ventilation!)) through the lung
We can measure the distribution of perfusion through lung using radioactive tracer (e.g. Xe133)
Inject into vein –> passes through lung
We will see a variation in blood flow between apex and base
The base of the lung receives grater perfusion than the apex
Total resting perfusion (Q.) of lung (5 litres/min) is distributed unequally through the lungs - base receiving 6 x more blood than apex.

19
Q

what is unequal distribution of perfusion through the lung due to?

A

Unequal distribution of perfusion through the lung is due to Gravity.
However, this is not to do with lung compliance, but how blood flows through vessels!
Schematic:
Blood flows into the lungs via the pulmonary artery with an arterial pressure
Blood flows out of lung with venous pressure
NB: there is also alveolar pressure that surrounds the vessels.
All pressures are given in cm of H2O (cmH2O)
You take the pressure at the tricuspid valve in heart as 0 (reference point)

20
Q

what is the pulmonary artery pressure at different levels??

A

The pulmonary artery pressure ~20 cmH2O at level of tricuspid valve - effectively 0
As you move down the lung, gravity causes ↑ in blood pressure (mass of blood adds pressure)
Moves linearly:
Base of lung is e.g. 20 cm below tricuspid valve - pressure ↑ by 20 cmH2O
Apex of lung is e.g. 20 cm above tricuspid valve - pressure ↓ by 20 cmH2O (no pulmonary artery pressure)
NB:
There is a ↓ in pressure as blood moves through lungs (as work is done to move blood so loss in energy is see as loss in pressure)
However the driving force (Pa - Pv) is constant at all levels - therefore blood will flow down its pressure gradient
Alveolar pressure = 0 when there is no air flow

21
Q

what happens in zone 3 (Pa > Pv > PA)?

A

Runs from the tricuspid valve to the base of lung
This zone has the greatest hydrostatic pressure due effect gravity:
Therefore, has a high arterial pressure 🡪 high venous pressure
Therefore has greatest blood flow
Here - Pa > Pv > PA
Therefore, driving force (blood flow) through flow in zone 3 is the arterial-venous difference
Here arterial-venous difference is barely changing so line is very steep (not much change in gradient) → blood flood is basically constant (second graph)
Alveolar pressure here is irrelevant, as it is always less then venous pressure

22
Q

what happens in zone 2: (Pa > PA > Pv)?

A

The Area above the tricuspid valve
Here Arterial pressure is falling 🡪 venous pressure is falling.
Alveolar pressure is still ~0,
Therefore, Venous pressure is now less than alveolar pressure
Pa > PA > Pv
Therefore, driving force of blood (blood flow) through zone to lung is now due to arterial-alveolar difference (NOT Pa-Pv difference)
As you move up from the tricuspid value towards the apex the a-A difference falls significantly 🡪 decrease in blood flow (second graph)
This eventually reaches a point where a-A = 0 🡪 here there is no more blood flow (as no driving force)
So, as we go up the lung we end up with alveolar pressure blocking blood flow through the lung.

23
Q

explain recruitment and distension?

A

Recruitment:
As seen in the graph above, as you move down zone 2 (from the apex - tricuspid valve) blood flow is increasing
This is because of recruitment:
As we move down zone 2 the a-A difference is increasing.
This increased a-A difference is able to recruit more blood vessels.
There are many pulmonary arterioles in the lungs which are collapsed as the A-a is too low to open them.
Because in zone 2, the a-A difference is greater towards the tricuspid valve than the apex, more vessels are recruited the lower down in zone 2 you are 🡪 increased flow as you move down zone 2.
For ZONE 3: Changes in blood flow occur due to distension.
In the entirety of zone 3 100% of vessels are open.
The lower down in zone 3 you are the greater the a-v difference.
This greater a-v difference results in a greater distention of the blood vessels –> greater blood flow occurs lower down Zone 3.
NB: Recruitment results in a greater increase in blood flow than distension

24
Q

what happens in zone 1: PA > Pa > Pv?

A

Zone one does not exist in healthy lung
Zone one occurs when PA > Pa
However, Zone 1 arises if:
Pulmonary arterial pressure falls (e.g. haemorrhage)
↑PA (e.g. positive pressure ventilation)
Therefore, in the case of a zone one, blood flow to the apex will cease totally (Pa < PA)

25
Q

explain why there is a ventilation/perfusion (V/Q) ratio

A

As described above both Ventilation (V.) and Perfusion (Q.) are NOT distributed equally through the lung:
The Base receives 2.5x more ventilation and 6x more perfusion than the apex
Therefore, if we plot the change in ventilation and perfusion across the lung on a graph:
We see that both ventilation and perfusion is greatest at the base of the lung, with Q.>V. at the base.
The fall in perfusion as you move towards the apex is greater than the fall of ventilation 🡪 so we reach a point where perfusion and ventilation are the same.
Thereafter V.>Q. and this continues to the apex of the lung
As a result V/Q is not equal across the lung:
V/Q is less than 1 at the base (0.6)
V/Q is greater than 1 at the apex (3.0)
V/Q = 1 at point of intersection
Average value of V/Q for the whole lung is around 0.8 (as majority of the lung is down towards the base).

26
Q

what is the physiological significance of V/Q variation?

A

Alveolar O2 + CO2 are determined by V/Q ratio
At normal V/Q of 0.8:
- PAco2: 5 kPa, PAo2: 13 kPa (so blood leaving this area will have these values)
- However, this is not consistent through the lung!

At V/Q of 0:
- No ventilation is occurring, but perfusion is still occurring
- This is a R-L shunt - blood passing through lung without oxygenation/removal of CO2
- PAco2 + PAo2 values will therefore be equal to venous values as this area equilibrates with venous blood.
- PAco2: 6 kPa = Pv co2
- PAo2: 5 kPa = Pvo2

At V/Q of infinity:
- No blood flow occurs but ventilation is occurring normally
- Theoretical! (unless you have total block of blood flow e.g., pulmonary embolism)
- This is therefore alveolar dead space ventilation, so alveolar values will be equal to room air:
- PAco2: 0 kPa = PIco2
- PAo2: 20 kPa = PIo2
- Because there is a continuum of V/Q (between 0 and infinity) across the lung our lung units/lobes can lie on this line.

27
Q

what happens if a lung unit has a V/Q of >0.8 or <0.8?

A

If a lung unit has V/Q ratio > 0.8 - the blood returning from that area will be higher in O2 and lower in CO2 than normal values (i.e. Pao2 > 13kpa & Paco2 < 5kpa)
If a lung unit has a V/Q ratio < 0.8 then blood returning from that area will be higher in CO2 and lower in O2 than normal.
So VQ ratio (set by variation in ventilation and perfusion) acts to set the alveolar O2 and CO2 which ultimately sets the arterial levels.

28
Q

what are the 2 mechanisms for the physiological adjustment of V/Q ratio?

A

2 mechanisms adjust V/Q ratio:
Alter bronchiole tone to alter V
Alter Arteriolar tone to alter Q

29
Q

what are the ways that diff areas of lung attempt to maintain the optimal V/Q ratio despite differences in their own ventilation/perfusion?

A
30
Q

how does hypoxic pulmonary vasoconstriction occur?

A

When the lung becomes hypoxic (low V/Q), it responds with active vasoconstriction (see on diagram as increase in blood pressure)
This diverts blood away from the hypoxic areas towards better ventilated areas
So, you end up with little blood flow where there is little ventilation
This also alleviates V/Q abnormality
This reflex response differs from every other systemic vessel:
Hypoxia, in anywhere else in the body, leads to vasodilation! (see in diagram as fall in BP)

31
Q

describe the process of vasoconstriction as a result of hypoxia

A

Vasoconstriction Mechanism:
Hypoxia inhibits the voltage gated K+ channels in the membrane of smooth muscle that surround the pulmonary artery.
This leads to membrane depolarisation –> opening of voltage gate Ca2+ channels –> influx of calcium –> pulmonary artery smooth muscle contraction (vasoconstriction)

32
Q

what does increased V/Q mismatch in lung disease cause?
how?

A

increased V/Q mismatch in lung disease causes low PaO2
V/Q Mismatch:
In a normal, young subject V and Q are well matched.
In a patient with bronchitis and emphysema:
V/Q are mismatched - do not have matching shape curves
There is Considerable blood flow (Q) to non-ventilated parts - low V/Q - functional shunt.
This leads to hypoxia (low Pao2) which will cause patient to breathe more.
As a result you get excessive ventilation in other parts of lung that have higher blood flow –> higher V/Q (in order to compensate for area where there is a low V/Q)
This is done to normalise hypoxia through trying to normalise Paco2

33
Q

Oxygen A-a difference ↑ with:

A

Excessive V/Q inequality
↑ a-v shunting
Impaired diffusion
These are things to think about when determining reasons for why a patient is low in arterial oxygen.
Is it due to them not breathing enough or is it because of some other problems (V/Q inequality, shunting or impaired diffusion)?

34
Q

what are the causes of V/Q mismatch affecting the whole lung and part of it?

A

Affecting whole lung:
- Pneumothorax
- Surgery on a single lung
- Congenital diaphragmatic hernia

Affecting part of a lung:
- Aspiration - inhale e.g. stomach contents into lungs
- Asthma/Bronchitis/Emphysema
- Pneumonia (infection)
- Pulmonary embolism
- Septicaemia (infection)
- ARDS or RDS of the new born

35
Q

give an example of finding the cause of Hypoxia (large A-a difference)

A

A 20 year old patient is breathing room air at sea level.
He has a Pao2 of 7 kPa and Paco2 of 8 kPa. R = 0.8.
The patient is hypoventilating (due to such a high Paco2 and a low Pao2)
But is this hypoxia due only to this reduce alveolar ventilation?
Such a high Paco2 of 8 kPa → shows hypoventilation is occurring
To see if other reasons for mismatch, use alveolar gas equation
Use the alveolar gas equation to calculate the ideal PAo2 - i.e. what it should be for the level of CO2 they have. It should be 9.5 kPa
Therefore, Pao2 should be much higher!
A-a = 9.5 – 7 = 2.5 kPa
This difference is excessive for patient’s age
Additionally, to hypoventilation there is ↑ V/Q mismatch (or ↑ shunt or impaired diffusion)
Other tests will be required to work out other cause.

If this 20-year-old patient’s PaCO2 was normal at 5.5kpa, would his V/Q mismatch be contributing more or less to his hypoxia.
Use alveolar gas equation to calculate pAO2
19.5 – (5.5/0.8) = 12.6
A-a: 12.6 – 7 = 5.6.
Therefore alveolar-arterial difference is a lot greater so V/Q mismatch is contributing more to his hypoxia.