What would you do...

[Bieber]

So, if I understand this correctly, the patient IS cyanotic, has present lung sounds with no wheezing, no signs of respiratory distress (accessory muscle use, nasal flaring, etc.), and is very tired and verbal. Based on his presentation, I'm gonna call him in respiratory failure and say this guy's about to go into respiratory arrest. I want to get him on the cot and raise the head of it so he's sitting up or at least at an incline, start assisting ventilations with a BVM and O2, and have another listen to lung sounds. If he's breathing that shallow, we probably didn't get a real great listen to his lungs. Now do we hear any wheezes, diminished sounds, rales/rhonchi?

Not going to spend too much time on scene, I want to get him out to the truck and get the monitor on him and start an IV NS TKO and do a quick 12-lead. I'd also like to go ahead and try an albuterol treatment regardless of lung sounds. Do we have any change in sats/condition/lung sounds with the ventilations and albuterol? Also, talking to family, has he been sick recently? And has this ever happened to him before? Has he ever had to be intubated before? I'm going to get my intubation equipment ready, but I'm going to hold off on tubing him if I don't have to.

Also, I'm a little confused about that ETCO2 reading. As I recall (and mind you, I'm sick so maybe I'm more confused than I realize), it would be hyperventilation that would cause that ETCO2 to be low, whereas hypoventilation would cause it to rise from the patient retaining so much CO2. So I'm a little baffled as to why his ETCO2 is only 31. I would expect him to be in respiratory acidosis, but that reading suggests the opposite. Though I guess bronchospasm or pulmonary embolism could cause low readings. So on that route, has he been bed bound for a while? Recent surgeries/trips or other PE risk factors? Any signs of a DVT? Also, do we have waveform with our ETCO2 and if so what waveform are we seeing?

[JakeEMTP]

Jumping into this one a little late and after reviewing the previous posts, I'd first sit the pt. up and reassess lung sounds. 02 via NRB initially while preparing a combivent. I'd hazard a guess that the pt. had attempted to self administer his prescribed Albuterol w/o relief. 12-lead ECG in the house get this guy to the ambulance. Let's start an IV and get 125mcg of Solumedrol on board. Capnography and begin transport emergency traffic. I'd be preparing my intubation and suction equipment, you know, just in case.

[D.P.Gumby]

[...]

Also, I'm a little confused about that ETCO2 reading. As I recall (and mind you, I'm sick so maybe I'm more confused than I realize), it would be hyperventilation that would cause that ETCO2 to be low, whereas hypoventilation would cause it to rise from the patient retaining so much CO2. So I'm a little baffled as to why his ETCO2 is only 31. I would expect him to be in respiratory acidosis, but that reading suggests the opposite. Though I guess bronchospasm or pulmonary embolism could cause low readings. So on that route, has he been bed bound for a while? Recent surgeries/trips or other PE risk factors? Any signs of a DVT? Also, do we have waveform with our ETCO2 and if so what waveform are we seeing?

I’ll take a whack at the low ETCO2 reading issue.

Two of the causes of poor concordance between PaCO2 and ETCO2 you mentioned: bronchospasm and PE (I suspect due to V/Q mismatch). However, COPD itself can also cause poor concordance, due to the already mentioned bronchospasm partially, but also due to an increase in deadspace and increasing V/Q mismatch.

This study of 118 COPD patients in the ED(I don’t have access to the full text, so I have to trust the abstract)

http://www.ncbi.nlm.nih.gov/pubmed/20224417

found:

“Mean arterial PCO2 levels were 43.24+/-14.73 and mean ETCO2 levels were 34.23+/-10.86 mmHg. Agreement between PCO2 and ETCO2 measurements was 8.4 mmHg and a precision of 11.1 mmHg.As there is only a moderate correlation between PCO2 and ETCO2 levels in COPD patients, ETCO2 measurement should not be considered as a part of the decision-making process to predict PaCO2 level in COPD patients.”

Similarly, this study (again, no full text for me) apparently found worsening concordance between PaCO2 and ETCO2 as degree of obstruction worsened:

http://www.ncbi.nlm.nih.gov/pubmed/18758420

There are several other similar but older studies with similar findings, all suggesting that ETCO2 cannot be trusted as an analogue of PaCO2 in those with cardiorespiratory disease.

One more, notably focused on prospective out of hospital use (though in Austria):

http://www.ncbi.nlm.nih.gov/pubmed/20224417

This all makes intuitive sense to me as well. We probably expect some degree of respiratory acidosis in COPD patients (especially the subset of “CO2 retainers”), and if these patients have systemic acidosis/hypercapnea due to inability to ventilate CO2, it makes sense that the level of CO2 escaping the pulmonary circulation and leaving the lungs to actually reach our ETCO2 detector could be lower than levels seen arterially.

I don’t think that low ETCO2 should necessarily increase our suspicion of PE without other indications, although I think your questions down that path are appropriate. Low ETCO2 readings are expected in COPD without other co-morbidities, and I don’t think that low ETCO2 is a particularly specific indicator of PE, at least not so much that my (inexperienced and very possibly wrong….) PE antenna go up with this patient. I think it’s far more likely that bronchospasm and mismatch/deadspace are the root of the lower than expected capnography readings.

[Bieber]

I'll take a whack at the low ETCO2 reading issue.

Two of the causes of poor concordance between PaCO2 and ETCO2 you mentioned: bronchospasm and PE (I suspect due to V/Q mismatch). However, COPD itself can also cause poor concordance, due to the already mentioned bronchospasm partially, but also due to an increase in deadspace and increasing V/Q mismatch.

This study of 118 COPD patients in the ED(I don't have access to the full text, so I have to trust the abstract)

http://www.ncbi.nlm....pubmed/20224417

found:

"Mean arterial PCO2 levels were 43.24+/-14.73 and mean ETCO2 levels were 34.23+/-10.86 mmHg. Agreement between PCO2 and ETCO2 measurements was 8.4 mmHg and a precision of 11.1 mmHg.As there is only a moderate correlation between PCO2 and ETCO2 levels in COPD patients, ETCO2 measurement should not be considered as a part of the decision-making process to predict PaCO2 level in COPD patients."

Similarly, this study (again, no full text for me) apparently found worsening concordance between PaCO2 and ETCO2 as degree of obstruction worsened:

http://www.ncbi.nlm....pubmed/18758420

There are several other similar but older studies with similar findings, all suggesting that ETCO2 cannot be trusted as an analogue of PaCO2 in those with cardiorespiratory disease.

One more, notably focused on prospective out of hospital use (though in Austria):

http://www.ncbi.nlm....pubmed/20224417

This all makes intuitive sense to me as well. We probably expect some degree of respiratory acidosis in COPD patients (especially the subset of "CO2 retainers"), and if these patients have systemic acidosis/hypercapnea due to inability to ventilate CO2, it makes sense that the level of CO2 escaping the pulmonary circulation and leaving the lungs to actually reach our ETCO2 detector could be lower than levels seen arterially.

I don't think that low ETCO2 should necessarily increase our suspicion of PE without other indications, although I think your questions down that path are appropriate. Low ETCO2 readings are expected in COPD without other co-morbidities, and I don't think that low ETCO2 is a particularly specific indicator of PE, at least not so much that my (inexperienced and very possibly wrong….) PE antenna go up with this patient. I think it's far more likely that bronchospasm and mismatch/deadspace are the root of the lower than expected capnography readings.

Great studies, man. Really informative stuff and thanks for sharing it. Where I work we only have ETCO2 for our ET tubes, so I don't get a chance to routinely monitor CO2 levels on the majority of my patients so it's getting fuzzy on me. And I agree that low ETCO2 readings in themselves don't really raise my index of suspicion for a PE all that much, however the fact that the patient APPEARS to have clear lung sounds (which as I stated above I want to confirm after I start ventilating via BVM) with such crappy O2 sats does put PE on my list of differentials. Especially if we get no increase in condition/sats with ventilation and no change in lung sounds following the albuterol (which I'm giving just in case they're diminished and I'm not picking up on it.) I'm not trying to look for zebras just yet, and once I know what kind of response I'm getting from the treatments above I'll be able to more finely tune my treatment and diagnosis, but I'm not ruling out anything just yet either and some of these findings make me wonder.

[JakeEMTP]

Beiber wrote:

however the fact that the patient APPEARS to have clear lung sounds (which as I stated above I want to confirm after I start ventilating via BVM) with such crappy O2 sats does put PE on my list of differentials.

Not trying to nitpick (seriously), unless I misread in the OP the pt. was moving some air and not very well if you ask me, but was negative for wheezing. Too bad the pt. is to weak to tolerate CPAP, that's what he needs IMHO.

Good conversation going here.j .,m

Edited January 7, 2011 by JakeEMTP

[tcripp]

Great input from everyone. Since this isn't a scenario game, per se, I can't tell you how things would have changed based on your interventions. What I can tell you is what I chose to do. I opted for a trip to the local facility for stabilization. That means that my treatment included BVM w/ 12 lpm O2 and diesel for 12 minutes. I am solo in the back, so I didn't get the opportunity to listed to lung sounds again during that time. However, by the time we arrived at the ED, his ETCO2 was 35 and his SPO2 was above 92. Don't remember the number off the top of my head.

Upon arrival, the ED sat him fully upright and gave him a neb treatment via NRB prior to my departure. The follow up I received was they eventually intubated him and flew him to a more appropriate facility 1.5 hours away (by ground). Heard that his ABG was 162...and that he is now home and doing well.

The one thing I didn't do that you've all pretty much said you would do...12-lead. Dang it!!! (lol...that's why I like this venue)

Wait til I post the one with elderly patient with a nose bleed and NO other symptoms who's EKG shows STEMI. Wow...

[JakeEMTP]

Wait til I post the one with elderly patient with a nose bleed and NO other symptoms who's EKG shows STEMI. Wow...

Damn! While that seems like a stretch, one of the reasons I pretty much acquire a 12-lead on all pt.'s except severe trauma (usually to much else going on). At minimum, all CP and SOB pt.'s get a 12-lead. It only takes a minute and you never know what you're going to get( with apologizes to Forrest Gump).

We had a pt. last shift who presented with 0 CP, non diaphoretic, no SOB, but just wasn't feeling "quite right". 12-lead showed he was having a Inferior MI.

[tcripp]

Damn! While that seems like a stretch, one of the reasons I pretty much acquire a 12-lead on all pt.'s except severe trauma (usually to much else going on). At minimum, all CP and SOB pt.'s get a 12-lead. It only takes a minute and you never know what you're going to get( with apologizes to Forrest Gump).

I may just start doing the same...

[Eydawn]

Man why couldn't I have worked with you guys prehospital... my thinking exactly about cardiac monitors. Damn my luck lol...

Great thread! I am still learning about VQ mismatch... that whole concept is very fuzzy to me.

Wendy

CO EMT-B

[chbare]

Man why couldn't I have worked with you guys prehospital... my thinking exactly about cardiac monitors. Damn my luck lol...

Great thread! I am still learning about VQ mismatch... that whole concept is very fuzzy to me.

Wendy

CO EMT-B

The VQ ratio is basically the amount of ventilation in and out of the lungs compared to the amount of circulation in and out of the lungs. A normal ventilation to perfusion ratio is about 4:5 or 0.8. Think about a person who has a minute ventilation of 4 litres per minute and perfusion through the lungs of about 5 litres per minute. In other words, ventilation through the lungs should approximate perfusion through the lungs. A ratio higher than 0.8 means there is more ventilation than perfusion and lower than 0.8 means that there is poor ventilation.

Take care,

chbare.