ETCO2 and PE

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82-Alpha599

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pt 66 y/o male, with 10 min downtime, huge cardiac hx. happened on the front lawn on a rainy day so we got into the bus to work on him (which I hate doing because now I have to transport either way). I got the tube and confirmed placement with lung sounds, condensation in the tube, syringe pull back without resistance, and good chest rise. pt started to pink up, but had a slow change in color on the ETCO2 detector.
I was wondering if he had a PE, would that cause the ETCO2 detector to change slowly because of bad O2 exchange in the lungs.

I asked the doc at the hospital and he said possibly but was unsure of himself. Ill ask one of the better docs when i get a chance but figured you guys would have something to say about this one.

ps. we dont have real capnography :sad:
 
82-Alpha599 said:
pt 66 y/o male, with 10 min downtime, huge cardiac hx. happened on the front lawn on a rainy day so we got into the bus to work on him (which I hate doing because now I have to transport either way). I got the tube and confirmed placement with lung sounds, condensation in the tube, syringe pull back without resistance, and good chest rise. pt started to pink up, but had a slow change in color on the ETCO2 detector.
I was wondering if he had a PE, would that cause the ETCO2 detector to change slowly because of bad O2 exchange in the lungs.

I asked the doc at the hospital and he said possibly but was unsure of himself. Ill ask one of the better docs when i get a chance but figured you guys would have something to say about this one.

ps. we dont have real capnography :sad:
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Possibly.

The colour change detectors are, in my experience, a bit variable and I certainly would avoid using them for anything other than tube placement in the seconds it takes to get a capnograph trace going.

Now, would a PE impair gas exchange to the point where ETCO2 would be noticeably changed. Maybe, but it would have to be pretty huge and there are a couple of variables that would have to be ruled out.
 
The ETT was placed after about 5-7 minutes of good CPR. Other times ive used the ETCO2 detector after about 3 breaths it was obviously yellow on exhalation.

and im guessing it was a pretty big PE (if it even was one). Big enough to kill him.
 
82-Alpha599 said:
The ETT was placed after about 5-7 minutes of good CPR. Other times ive used the ETCO2 detector after about 3 breaths it was obviously yellow on exhalation.

and im guessing it was a pretty big PE (if it even was one). Big enough to kill him.
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Did they autopsy him? Check with your medical director to see if he can request the medical examiner's findings on the case. We used to do it all the time for any case that resulted in death. It can be a very valuable way to check to make sure we are accurately identifying issues that we think we are seeing.
 
It could be the detector, it is possible that it was a PE too. With a PE, capenography will yield a low number, i.e. less CO2 getting out than normal, so theoretically, with less CO2 coming out, it could take longer for the colorimetric device to change. Whether or not there is data to back that up, I couldn't tell ya.
 
Now, I admit, I'm still a little shaky on this info. So if I'm wrong, please correct me.


If you're using capnography on a tubed patient, isnt the ETCO2 representative of the probably outcome of the patient? ie - Aren't tubed patients with ETCO2 of around 35-45 a good candidate for working and ROSC because of the proper gas exchange going on, and meanwhile a patient with ETCO2 of 10-12 has a poor prognosis?

Therefore, lower ETCO2 would equate to a poor change in color on the detector. Therefore, showing you that gas exchange is happening, just not well, and it may not be a PE, it may just be because the man is dead.



Also, you should probably have capnography, being the "gold standard" and all. But it can be expensive. =/
 
MonkeySquasher said:
Now, I admit, I'm still a little shaky on this info. So if I'm wrong, please correct me.


If you're using capnography on a tubed patient, isnt the ETCO2 representative of the probably outcome of the patient? ie - Aren't tubed patients with ETCO2 of around 35-45 a good candidate for working and ROSC because of the proper gas exchange going on, and meanwhile a patient with ETCO2 of 10-12 has a poor prognosis?

Therefore, lower ETCO2 would equate to a poor change in color on the detector. Therefore, showing you that gas exchange is happening, just not well, and it may not be a PE, it may just be because the man is dead.
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Correct, EtCO2 less than about 10-12 after 10 minutes pretty much means there is no likelihood of a good outcome. I wouldn't necessarily expect numbers of 35-45 in an arrest but good CPR should give reasonable numbers. Can't post references on my iPhone sorry

Also, you should probably have capnography, being the "gold standard" and all. But it can be expensive. =/[/QUOTE]
 
You mentioned it was raining. Any chance your ETCO2 detector got wet?
 
I don't have the link but I remember reading a study on ETCO2 in cardiac arrest as a predictor or survival, and no pt. with an ETCO2 of 10 or less survived.

In PE, you can expect the pt.'s ETCO2 to be lower than normal because a smaller section of the lungs is participating in gas exchange, thus the volume of exhaled CO2 will be less.

And ditto before, your service NEEDS waveform capnography. No argument about it. It's the gold standard and it's shameful that any service allowing advanced airway placement doesn't have it.
 
I wanted to add on that it's possible to see an ETCO2 reading of 1-2mmHg and still have your tube in the trachea, in a "low-flow" situation. Rely on the waveform itself, not necessarily the mmHg reading. This is another reason why you need waveform capnography and not just a colormetric device.
 
Also remember, if you don't have good gas exchange through the capillaries (ie... PE) it is going to be EVEN HARDER for you to lower your ETCO2 and raise your SPO2.
It is already tough to lower the ETCO2 in an arrest because the Co2 has a 200X affinity to the hemoglobin. Especially someone who has been down for 10 min and is already in acidosis. So with a blockage that potentially killed this guy, you have to also think that the blockage was big enough to cause a more difficult time raising your SPO2 and lowering your ETCO2.
 
SoCal said:
Also remember, if you don't have good gas exchange through the capillaries (ie... PE) it is going to be EVEN HARDER for you to lower your ETCO2 and raise your SPO2.
It is already tough to lower the ETCO2 in an arrest because the Co2 has a 200X affinity to the hemoglobin. Especially someone who has been down for 10 min and is already in acidosis. So with a blockage that potentially killed this guy, you have to also think that the blockage was big enough to cause a more difficult time raising your SPO2 and lowering your ETCO2.
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I think you mean carbon MONOXIDE has 200x the affinity to hemoglobin.
 
You are totally correct. I apologize^ however Co2 does bind to proteins on the hemoglobin and can inhibit the carrying of Oxygen.

Also if there is a blockage, the blood flow doesn't even get to the alveoli to get exchanged. This hampering the body's ability to get Co2 out and O2 in.
 
While you are correct about the affinity, being CO and not Co2, you also need to remember that if your pt has a downtime of >10 min and is already acidotic then you run into a problem.

When the atmosphere in the vascular system is so acidotic, the O2 molecules will not off load in the capillary beds like they are supposed to, thus remaining a high Co2 retention and high ETCO2.
 
SoCal said:
While you are correct about the affinity, being CO and not Co2, you also need to remember that if your pt has a downtime of >10 min and is already acidotic then you run into a problem.

When the atmosphere in the vascular system is so acidotic, the O2 molecules will not off load in the capillary beds like they are supposed to, thus remaining a high Co2 retention and high ETCO2.
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One of our RTs correct me if I'm wrong, but I think you might want to review respiratory physiology, particularly the oxygen dissociation curve and the Bohr effect. Acidosis causes a rightward shift, not leftward.
 
Smash said:
One of our RTs correct me if I'm wrong, but I think you might want to review respiratory physiology, particularly the oxygen dissociation curve and the Bohr effect. Acidosis causes a rightward shift, not leftward.
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Simply put, and not to get down to the minute details, your hemoglobin and the proteins that make up the hemoglobin, work in a homeostatic environment, with the acidotic OR alkalotic environment, the hemoglobin WILL NOT offload the needed o2 molecules to the cells, hence carpal pedal spasms and a hypoxic environment at the cellular level. End of story.

And the pt. having a downtime of >10 min. provides the correct situation for the acidosis to occur. This having a direct affect on the O2 and CO2 transfer and your ETCO2 readings.
 
Smash said:
One of our RTs correct me if I'm wrong, but I think you might want to review respiratory physiology, particularly the oxygen dissociation curve and the Bohr effect. Acidosis causes a rightward shift, not leftward.
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You don't need to be an RT to know that a right shift causes and increase of offloading of O2 to the cellular tissues. It also requires a higher partial pressure of O2 to bind to the hemoglobin; however

this is how COPD'ers are able to maintain cellular respiration, because they are slightly more acidotic, their tissues still receive oxygenation.

What were the lung sounds on this patient? Strangely enough, the patient's i've cared for with PEs had diminished lung sounds over the affected area.
 
SoCal said:
Simply put, and not to get down to the minute details, your hemoglobin and the proteins that make up the hemoglobin, work in a homeostatic environment, with the acidotic OR alkalotic environment, the hemoglobin WILL NOT offload the needed o2 molecules to the cells, hence carpal pedal spasms and a hypoxic environment at the cellular level. End of story.
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Sorry, but that is just not the case. In an acidotic environment, O2 dissociates more easily from haemoglobin (the Bohr effect), ensuring improved delivery of O2 at the tissue level --> the haemoglobin 'offloads' the O2 more readily. It does, as jimi points out, require a higher partial pressure of O2 at the lungs. In an alkalotic environment O2 does not dissociate as easily from haemoglobin. This is depicted with the oxy-haemaglobin dissociation curve.

This is what maintains homeostasis. There are no doubt people who can explain this far better than I, but I would have thought that this would be basic paramedic level physiology.

And the pt. having a downtime of >10 min. provides the correct situation for the acidosis to occur. This having a direct affect on the O2 and CO2 transfer and your ETCO2 readings.
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Yes, but not necessarily just increasing EtCO2. Initially there will most likely be a higher than normal EtCO2 reading when you start CPR essentially from 'washing out' the accumulated CO2 from when the body was going from a low to no flow state. However, to produce CO2 (and thus a reasonable EtCO2 reading) you need to have perfusion. A cardiac arrest patient, by definition, does not have perfusion. We should be able to maintain some perfusion with CPR and to some extent with pressors, but it will be typically lower than normal. The issue is not lowering EtCO2 in cardiac arrest, but raising it. This is why there is a direct correlation between EtCO2 levels and survival from cardiac arrest: EtCO2 represents perfusion, no perfusion equals no survival.

With a large PE you must also have a lower than 'normal' EtCO2 reading, because you have a large amount of alveolar dead space.
 
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