# capnography questions



## zzyzx (Nov 22, 2011)

1) Why would the ETCO2 be decreased in a patient with a big pulmonary embolism? I can understand why in a small PE the ETCO2 would be a lower value due to hyperventilation, but shouldn't the ETCO2 be high in a big PE due to a severe V/Q mismatch?

2) The ETCO2 will match the PaCO2 in a healthy patient. Why might it not correspond in a person with cardiovascular issues?

3) It is correct that in a patient with severe pulmonary edema the ETCO2 would be elevated, right?


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## Dwindlin (Nov 22, 2011)

1.  In massive PE you have increased dead space where no gas exchange is occurring.  Alveolar values begin to approach that of room air (high O2 low CO2).

2.  In conditions such as cardiogenic shock less CO2 is delivered to the lungs and thus can decrease EtCO2 values (You can have other EtCO2 changes due to cardiac conditions this is just one example).

3.  Yes.  


zzyzx said:


> 1) Why would the ETCO2 be decreased in a patient with a big pulmonary embolism? I can understand why in a small PE the ETCO2 would be a lower value due to hyperventilation, but shouldn't the ETCO2 be high in a big PE due to a severe V/Q mismatch?
> 
> 2) The ETCO2 will match the PaCO2 in a healthy patient. Why might it not correspond in a person with cardiovascular issues?
> 
> 3) It is correct that in a patient with severe pulmonary edema the ETCO2 would be elevated, right?


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## Dwindlin (Nov 22, 2011)

Sorry to quote my own post.  But my I need to correct something and I can't edit the post.

For number 3 if it is pure pulmonary edema (i.e. not cardiac) it EtCO2 will decrease via the explanation for number 1.  Cardiac pulmonary edema will show a rise.



Dwindlin said:


> 1.  In massive PE you have increased dead space where no gas exchange is occurring.  Alveolar values begin to approach that of room air (high O2 low CO2).
> 
> 2.  In conditions such as cardiogenic shock less CO2 is delivered to the lungs and thus can decrease EtCO2 values (You can have other EtCO2 changes due to cardiac conditions this is just one example).
> 
> 3.  Yes.


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## Trevor (Nov 23, 2011)

okay so, large pulmonary embolisms can effect ETCO2 several different ways, all resulting in decreased ETCO2 readings...

1) A large clot will block blood going to the lungs and create hypoxia. If the blood is hypoxic, then gas exchange can not occur, leading to hypocapnea. 

2) If someone arrests from a PE (like any other type of arrest) they will be in a low perfusion state. This will again result in hypocapnea, due to poor perfusion, and hence poor gas exchange. 

3) like stated above, multiple PEs, like in a "Shower" can create alveolar dead space, which can lead to decreased gas exchange also...


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## systemet (Nov 24, 2011)

I was going to write a long post in response to this, but I found a webpage, written by a Canadian CCP, that does a far better job:

http://www.paramedicine.com/pmc/End_Tidal_CO2.html

You've got to bear in mind with these situations that what we're really interested in is the amount of CO2 in the arterial blood, the PaCO2.  CO2 diffuses very quickly, and if we consider an alveolus that's perfused, the partial pressure of CO2 in the alveolus (PACO2) is pretty much equal to the pressure in the surrounding capillaries.  

* If we could always measure this value, it would be fantastic.

Unfortunately, when we're measuring capnography, we're also measuring the CO2 content of air from alveoli that are ventilated, but not perfused.  These will have lower amounts of CO2 than are present in the arterial system, and will lower our reading.

[This discrepancy between perfusion and ventilation is often referred to as VQ mismatch]

As a result, in healthy people, our recorded ETCO2 is usually a little lower than PaCO2.  Somewhere around 3-8 mmHg lower.

Now, this wouldn't be too bad.  But a lot of the people we deal with are sick, especially the respiratory disease patients, and this difference can often be much greater, to a point where the PETCO2 reading is almost meaningless.  We might have someone with a PaCO2 of 55, and a PETCO2 of 30.  Our recording device is suggesting that we're hyperventilating the patient, but actually, they're hypercapnic.  A simple situation may occur when cardiac output is decreased, e.g. cardiac arrest, shock, hemorrhage, etc. or perfusion is otherwise disturbed (e.g. PE).  

We can also see the relationship go the other way, with a higher PETCO2 than the corresponding PaCO2 measured by ABG, if our patient is hypothermic -- as CO2 solubility differs with temperature, and ABGs are corrected to 37C. 

There's a lot of research out there, I can link to some if you guys would like, although most of it requires a university log-in.  But if you start looking at real numbers in patients seen in the ED or transported by EMS, there's a very poor correlation between ETCO2 and PCO2.  So while these numbers are the best measure of ventilation that we have, I don't think they're as useful as we're often made to believe in paramedic school.


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## usalsfyre (Nov 24, 2011)

sysemt covered most of what I was going to say pretty well. A couple more points to consider though. First, ETCO2 is also reflective of alveolar and airway status as well. In addition ETCO2 is immensely more useful (not that it's not useful anyway) on an IFT when you've got a ABG. As long as hemodynamic and alveolar status don't change the gradient will remain the same. Meaning you have a very accurate window to PaCO2. Another point to consider is that oxygen delivery often causes some "washout" of CO2 in the hypopharynx  so the sample off of a NC might not be accurate. 

Many paramedics and paramedic instructors aren't taught this and go off of only what the rep tells them. ETCO2 is a wonderful tool if you understand its limitations.


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## Sam Adams (Nov 25, 2011)

http://emscapnography.blogspot.com/

Here's another rescourse for y'all


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## zzyzx (Nov 26, 2011)

Thanks for all the responses. Geez, after years of using capnography I'm realizing I never understood some fundamental concepts.

Just to be sure I'm getting it right finally, if there is a ventilation-perfusion mismatch, and the problem is with perfusion, as in a big PE or cardiac problems, the ETCO2 numbers will likely be lower than the actual PaCO2. Correct? If on the other hand the alveoli are getting great perfusion but aren't getting ventilated properly, as in bronchospasm or non-cardiogenic pulmonary edema, the ETCO2 will accurately reflect the PaCO2 and will show a high number.


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