Ventilation/Perfusion Flashcards

1
Q

total exhaled ventilation

A

Ve

  • Total amount of ventilation in and out of lung at any moment, or averaged over time. Called Total Exhaled Ventilation.
  • Why exhaled? Don’t want to confuse with TV (total or tidal volume). Also, in the laboratory most measurements are taken with respect to exhaled
  • Ve can be broken into two components:
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2
Q

Dead space ventilation

A
  • Dead Space Ventilation (Vd): ventilation stuck in airway and cannot participate in gas exchange, which only occurs in the alveolus.
  • Its functionally dead in terms of gas exchange but that portion of the lung is alive and well.
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3
Q

Alveolar ventilation

A

•Alveolar Ventilation (Va): Component that makes it down into the alveolar air space. It is the component that’s responsible for the uptake of O2 into the blood and the excretion of CO2.

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4
Q

Relationship between 3 types of ventilation

A

Va = Ve - Vd

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5
Q

What does total ventilation reflect?

A

work performed by respiratiory system

•The total ventilation reflects the work that your respiratory system is performing. Very clinically relevant; SOB (dyspnea) is considered to be an elevated or increased work of breathing until it becomes uncomfortable. Work load has to reflect total ventilation.

Brain can only control output the muscle which controls total ventilation. Cannot control only alveolar ventilation

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6
Q

what does dead space ventilation reflect?

A

vol of ventilation that does not participate in gas exchange

25% of TV in normal subjects - increased by disease

•Dead space does not participate in gas exchange and accounts for approximately 25% of the tidal volume for those of us sitting in the room. A normal tidal volume might range from 500-600, the dead space volume is around about 125-150 ccs and so if you divide those 2 numbers you will come up with about 25% of the tidal volume. That 25% is an insufficiently in the system. It becomes increased in a variety of pulmonary diseases; thus we want to measure as an indication of how much insufficiency a patient has.

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7
Q

what does alveolar ventilation reflect?

A

volume of ventilation that participates in gas exchange! most important for determinng arterial PCO2

•Alveolar ventilation participates in gas exchange. It is very important in determining the arterial partial pressure for CO2.

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8
Q

measurement of dead space ventilation

A

inspiration - no CO in dead space (at end of inspiration!)

in expiration - volume exhaled is diluted by volume of dead space -

  • At end of inspiration there is no Co2 in dead space volume because there is no gas exchange. To measure dead space we allow subject to exhale and collect exhaled gas in chamber. Shown in end of expiration diagram on right.
  • Lung volume is now smaller, dead space volume now has Co2 in dead space because when first aliquot of air came out of lung that is air already in the airways (no Co2). As patient continues to exhale you have alveolar gas entering through airways such at there is a partial pressure of Co2 in the airways that is present and measurable.
  • Fraction of Co2 in airway should be the same as fraction in alveoli. Looking at exhaled chamber (in box), there will be a lower fraction of Co2 because it includes dead space volume (that has no Co2) mixed with alveolar volume (which has Co2) resulting in a lower Co2 fraction than that which was present in alveolar gas.
  • Thus, the concentration of Co2 in exhaled gas reflects how much alveolar gas is diluted by the dead space.
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9
Q

equation for measurement of dead space

A

VD/VT = (PaCO2 -PeCO2)/PaCO2

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10
Q

measurement of alveolar ventilation

A

measure dead space ventilation (using exhaled PCO2) and then subtract from total ventilation

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11
Q

equation for the arterial pressure of CO2

A

metabolic CO2 production/alveolar ventilation

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12
Q

•How do we measure total volume of Co2 being produced all over body?

A

•At STEADY STATE, it has to reflect the volume made at tissues. Thus, metabolic Co2 production equals volume of exhaled Co2 at steady state.

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13
Q

how do we measure CO2 production?

A

volume of exhaled CO2 = total exhaled ventilation x PP CO2 in air

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14
Q

alveolar ventilation equation

A

PaCO2 = K x VCO2/VA

VCO2 can be estimated by body size and metabolic state

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15
Q

In a healthy subject, what would 50% increase in metabolic rate do to arterial PCO2?

A

nothing! body compensates

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16
Q

hyperventilation

A

reduced arterial CO2

must occur due to an increase in VE since VD can’t change

  • Low pCo2 is alveolar hyperventilation. Only way occurs is if alveolar ventilation goes up and only way to do that is to increase total ventilation because can’t selectively reduce dead space.
  • Low pCo2 is probably most common blood gas abnormality you will encounter in clinical medicine. If you take people with resp. disease most common finding is low pCo2. Reason is not known but probably due to a variety of factors including probably a variety of receptors in lung parenchyma that feedback to resp. control system via vagus nerve and result in increase in ventilation. Normal response to a disease, and if a patient chooses to breathe at an elevated ventilatory rate, so be it. But nothing of interest in terms of an abnormality in the system.
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17
Q

hypoventilation

A

elevated arterial CO2

may occur due to decreased VE or increased VD

  • More interesting phenomenon is when pCo2 goes up because that tells you that there is failure of the respiratory system to excrete Co2 and that is a type of resp. failure that you’ll learn next week. Does pCo2 go up because reduction in ventilation or increase in dead space?
  • Lung disease reduces ventilation and increases dead space. Neuromuscular diseases generally result in reduced ventilation. Sleep also reduces ventilation, but metabolic rate also goes down. But the drop in ventilation is larger than drop in metabolic rate. pCo2 goes up 4, 5 or 6 mmHg in normal adults during sleep.
  • Increase in dead space is generally attributed to disease states.
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18
Q

neuromuscular disease

A

drop in ventilation because can’t do effort

19
Q

lung disease

A

drop in ventilation

20
Q

hypoventilation - heroin overdose

A

elevated CO2

decrease in VE - proportional decrease in VD and VA

ratio of dead space stays the same!

21
Q

hypoventilation - COPD at rest

A

CO2 is increased

VE is high - so is VD and VA

VD is disproportionally high - much bigger ration, need more VE to get to get VA

22
Q

hypoventilation - COPD on big breath

A

hugh increase in VE

HUGE VD

can raise VA and lower PCO2 enough but still have really high percent of dead space

23
Q

how to assess level of ventilation

A

look at pCO2

24
Q

how to assess oxygenation

A

measure PO2, pH

calculate O2 sat

25
Q

mechanisms of hypoxemia

A

V/Q mismatch

hypoventilation

shunt

diffusion impairment

low inspired O2

26
Q

Equation for inspired PO2

A

FIO2 x (Pb - Ph20)

1) The first is the inspired PO2. We can calculate that by taking the FIO2, which is the fraction of O2 in the inspired air, and multiply by barometric pressure. We know that ambient air is about 21% O2 and we can multiply that by the barometric pressure to come up with an estimate of the inspired O2 but first you’ll notice I have subtracted the partial pressure of water, water vapor pressure. And the reason for that, I think Dr. Munger had mentioned is that one of the important functions of the upper airway is to humidify gas as we’re breathing. And so you know as we’re breathing, breath by breath your upper airway and oral pharynx is doing a very efficient job of humidifying the inspired air. In fact the inspired air becomes fully saturated with water. That prevents drying of mucous membranes and tracheobronchial tree which produces irritation and inflammation if it’s not present. And so if I want to calculate the fraction of O2 in the inspired air I have to first subtract the water vapor pressure from the barometric pressure.

So for us sitting here in the auditorium, we are at sea level. Barometric pressure is about 760 mmHg. PH2O (at body temperature which is 37°C) when you’re fully saturated = 47 mmHg. So 760-47 = 713. If I multiply that by .21 for fraction of inspired O2 it’ll calculate that the inspired PO2 = 150 mmHg. So for all of us sitting in this room the inspired PO2 = 150 mmHg and that’s a nice number to remember and I’ll show you why as we go through the lecture.

27
Q

perfect V/Q matching

A

The amount of ventilation entering the alveolus per unit time is exactly equal to the amount of blood flow coursing by it

28
Q

perfect ventilation of alveolar/cap interface

A

Full equilibration of partial pressures of the gases in the alveolar air space with capillary blood.

29
Q

stead state gas exchange

A

the total amount of O2 uptake for all the cells of the body would equal the amount or quantity of O2 uptake in the lung from the alveolus to the capillary. And of course similarly for the CO2 production by the cells and in CO2 excretion in the lung.

30
Q

respiratory quotient

A

ratio of how much CO2 is produced relative to O2 consumed.

The respiratory quotient gives you the proportionality of how much CO2 is produced for each quantity of O2 that’s consumed.

For a typical diet we’re somewhere in between these two extremes and normally R = 0.8. For us sitting here in steady state conditions this number is going to be very important when we talk about alveolar gases.

31
Q
A

We would take the inspired O2 of 150 and we know that it’s going to fall roughly by how much the alveolar CO2 goes up. So we subtract off from the 150 the PACO2. We have to do one thing first which is remember that the exchange for CO2 is not 1 for 1. It’s dictated by the R so I want to account for that difference and so I dived the PACO2 by the R so I have the proportionality correct. So in fact I can calculate how much PO2 falls by measuring how much it’s replaced by PCO2. Now this is alveolar CO2 in this equation but remember we can use the arterial CO2 as a surrogate because they’re essentially identical clinically. There’s always full equilibration between alveolar and arterial PCO2.

32
Q

shunt

A

i.e. pneumonia

because there’s no gas flow coming into the lung. And so in fact we can take our simplified model of a lung and opacify the alveolus, there’s no air, and therefore the mixed venous blood is identical to the capillary blood. This is blood that’s shunted not coming into contact with inspired air.

Now the example I’m showing here is an intrapulmonary shunt because blood flow is going through the lung but not coming in contact with air. One can have other types of shunting. For example, intracardiac shunting. So if you have a septal defect you can have shunting across the cardiac septum. Most commonly would be the atrial septum than the ventricular septum. So one could get both intracardiac or intrapulmonary shunting. This is an example of intrapulmonary shunt.

33
Q

Dead Space V/Q

A

i.e. PE

You have inspired gas that’s entering this unit. There’s nothing preventing the flow of O2 into this alveolus but there’s no blood coming passed it. And so this inspired gas has no effect on the gas tensions in the blood because there’s no blood flowing passed that unit. There’s no gas exchange. Remember how we defined dead space. We defined it as inspired air that does not participate in gas exchange. So this is a dead space. Here’s another example of how dead space exists in the alveolus as opposed to simplistically thinking about conducting airways.

Now I promise you that these are two different extremes of ventilation-perfusion relationships. [switches back to slide 11] So if in the ideal situation we talk about ventilation to perfusion ratio which is 1…[switches to slide 13] in the shunt, the ventilation is 0 but there’s ongoing perfusion so the VQ ratio is 0. [switches back to this slide] And here in the dead space we have ongoing ventilation but no perfusion so the VQ ratio becomes infinity. And so you have you’re ideal 1 and two extremes going from 0 to infinity.

34
Q

distribution of pressures

A

IPP more negative on apex

weight of lung sitting on base - making it less negative

35
Q

distribution of alveolar size

A

Now that gradient of pleural pressure has a significant impact on alveolar air size. A typical alveolus at the lung base is subject to a transpulmonary pressure of 0 in the alveolus relative to -2.5 in the pleura, a 2.5 cm transpulmonary pressure as compared to a similar alveolus up in the apex where transpulmonary pressure is 10 because the intrapleural pressure is a little bit more negative. And so alveolar size in the apices are a little bit larger than they are at the base simply because of the pleural pressure gradients.

36
Q

Distribution of ventilation

A

alveoli are smaller at the bottom - but at this point of the presure-volume curve, alveoli are more easily distended

Now this may seem a little problematic because I’ve already told you that most of the ventilation is actually going toward the base of the lung. Why is it that most of the ventilation is going to the alveolus that’s actually smaller? The reason is you have to think about these alveoli as you think about the volume pressure relationship of the lung. The one that’s at the base is starting at a transpulmonary pressure of 2.5 as compared to the alveolar unit at the apex starting at a transpulmonary pressure of 10. And you’ll notice that the one at the base is starting at a much steeper part of the volume pressure relationship than the alveolar units at the lung apices. So for any given muscle pressure, a delta P that you may generate, you’re going to get a bigger change in volume at the bases than you are the apices.

37
Q

VQ rate along vertical axis of lung

A

So if I calculate the ventilation perfusion ratios, which is just these two lines, it’s not going to be a constant number throughout your lungs. And I can graph this with the yellow line with the numbers on the right axis. At the base of the lung, ventilation is low relative to the blood flow. The ratio is somewhere around 0.6. At some point the two curves cross and here ventilation and blood flow are equal, I get a V/Q ratio of 1. And as we move up to the apex, because the blood flow is falling faster than the ventilation, I start to get elevated V/Q ratios of over 3 at the lung apex.

38
Q

apex V/Q

A

At the apex V/Q ratio is about 3.3 meaning there’s lots of fresh air entering the alveolus relative to blood flow. That means we’re replenishing the alveolar air space with a high PO2 gas quite readily. And therefore the PO2 in the alveolar air space is going to be high, a number like 132. Because ventilation is high, CO2 excretion is going to be quite vigorous and the PCO2 is going to be lower than normal, a value of 28.

39
Q

V/Q at base

A

When we go down to the base of the lung, I’ve shown you that the V/Q is going to be lower, about 0.6, meaning there’s less inspired air coming in and so the inspired partial pressure in the alveolar air space is going to be lower. And in this example it comes down to about a value of 89. The PCO2 will be correspondingly higher at 42 and of course the oxygen content is going to be lower and will be 19.2.

40
Q

how to calculate mixed venous blood

A

The key thing to remember is you’re not mixing partial pressures. You’re mixing content. For every 100dl of blood in a healthy lung, I have 18.6ml of O2 and for every 100dl in a diseased lung I have 16.0ml and those two numbers is what you need to average.

average the O2 content (not saturation or pressure)

compensation - hypoxic vasoconstriction! actually closer to higher PO2

41
Q

alveolar-arterial O2 diff

A

calculate ideal alveolar PO2

are taking the ideal value, this is the best my patient could achieve, and I am going to see how close the arterial blood is to that idea

use alveolar air equation (150-PaCO2/.8)

42
Q

how to calculate oxygenation

A

A-a O2 diff with ideal alveolar

43
Q

how to calculate ventilation

A

PaCO2 and VE

use alveolar ventilation equation

44
Q
A