ETCO2 of 9

[Simusid]

I was on a call recently for an unresponsive female with an unknown downtime. HX of ETOH abuse and family members stated "she was on meds for it", there was no evidence of alcohol on scene. Nor an evidence of an overdose

She remained unresponsive, had irregular respirations at a rate of about 10, a pulse of about 120, O2 SAT of 100%. I don't remember the BP but it was not hypotensive. She also had some moderate irregular jerking of her right side limbs. My partner said "drug overdose or a head bleed...lets go" and we did. At the hospital, it was discovered (by the family) that she actually drank brake fluid.

The thing I don't understand is that her ETCO2 was 9. She had a perfusing rhythm and had some level of respiration (though inadequate, she ended up being tubed). Satting 100% she was moving blood and air....why would her CO2 be only 9? could the brake fluid interfere with that measurement?

 

[NYMedic828]

Ethylene glycol is highly toxic to humans if ingested.

Was she drinking it in a suicide attempt? I can't imagine anyone drinking a substantial amount by accident...

 

[ThadeusJ]

What was the waveform like? It would have been interesting to see what the ABG's were so you could correlate the gradient. How was the EtCO2 measured (prongs?). Were they compromised with secretions?

 

[Simusid]

What was the waveform like? It would have been interesting to see what the ABG's were so you could correlate the gradient. How was the EtCO2 measured (prongs?). Were they compromised with secretions?

Sorry I did not see the waveform, only the number. I'm fairly sure there were no significant secretions.

 

[fast65]

I know someone asked this already, but how was the ETCO2 measured? Was it through a nasal cannula, or was it monitored after she was intubated?

If she was breathing primarily through her mouth, then you'll obviously have a skewed reading if you're using a cannula to monitor capnography. That being said, I would also like to see the ABG's.

 

[Simusid]

I know someone asked this already, but how was the ETCO2 measured? Was it through a nasal cannula, or was it monitored after she was intubated?

If she was breathing primarily through her mouth, then you'll obviously have a skewed reading if you're using a cannula to monitor capnography. That being said, I would also like to see the ABG's.

It was measured with a NC on a lifepak 15

 

[NYMedic828]

It was measured with a NC on a lifepak 15

That measurement may or may not be accurate then. When she was intubated it should be re-assessed via the ET tube to see how close the numbers are.

The NC type has too many variables to be completely accurate. Anything from secretions blocking the prong to exhaled air simply coming out of the mouth vs the nose can affect the reading.

Its an extra tool its not very good for more definitive measurements. Kinda like pulseoximetry.

 

[STXmedic]

I'm not sure what kind of EtCO2 cannulas y'all use, but the ones we use here have a piece below the nasal prongs that sits in front of the mouth and captures the air exhaled from the mouth.

So depending on what type of cannula the OP uses, mouth breathing may or may not affect the end-tidal reading.

 

[Tigger]

I'm not sure what kind of EtCO2 cannulas y'all use, but the ones we use here have a piece below the nasal prongs that sits in front of the mouth and captures the air exhaled from the mouth.

So depending on what type of cannula the OP uses, mouth breathing may or may not affect the end-tidal reading.

That's what we use and unless the patient is forcibly exhaling through their mouth they are still accurate.

 

[RustyShackleford]

We use the same type as noted above and they have always been pretty accurate when compared to in hospital/ETT readings.

 

[Melclin]

ETCO2 is generally only considered to be a reliable indicator of PCO2 in young people who aren't super crook. Derangement of cardiac output and lung function effect it.

Here is a nice short doc on ETCO2 with reference to V/Q.
http://www.procamed.ch/pdf/etco2_gradient.pdf

Probably falsely low though due to some oddity of the equipment (as others have already mentioned), which would be impossible to say without




A good resource for capnography.

http://emscapnography.blogspot.com.au/

 

[jwk]

We use the same type as noted above and they have always been pretty accurate when compared to in hospital/ETT readings.

No, they are not. Using the numbers from any system that monitors EtCO2 from a nasal cannula is pointless.

 

[Simusid]

So far the responses seem to be questioning that the ETCO2 measurement is wrong. I get that, and I do not blindly treat numbers.

But my question is more about physiology I think. Suppose hypothetically that the number was correct. What could be going on in her body to cause this low reading?

 

[ThadeusJ]

You have to consider what you are looking for. Reading an airway sample of CO2 assumes a correlation with pulmonary vascular PCO2, which assumes a correlation with systemic PCO2 and cell function. Therefore, if the machine is reading correctly, one can consider a V/Q mismatch where the CO2 in the pulmonary vasculature is higher (severe bronchoconstriction). If the CO2 in the pulmonary vasculature is in fact low, then there could be a issue such as shunting of the blood from the right side to the left side of the heart, bypassing the pulmonary system, in which case the systemic PCO2 is higher than the pulmonary PCO2. An ABG would detect that as well.

If the patient is hyperventilating and the system is working properly, then the systemic PCO2 would be low as well. I can't think of why cellular PCO2 would be high and not diffuse into the systemic bloodstream. I suppose there could be a cataclysmic shift of the Henderson Hasselbalch equation where the PCO2 leaves the system to form bicarb, (I think that was the mechanism in the Fantastic Four when Thing was created, but I digress).

 

[46Young]

A few days ago I ran a teenage girl at school for abdominal pain. When we arrived, she was hyperventilating north of 40/min. Her B/P was roughly 110/62, P 80, SpO2 100% RA per the engine crew initially. The engine crew had her on an NRB with 2lpm, presumably so that she would rebreathe her CO2. My EMT-I partner who was riding lead cranks up the O2 to 10 LPM's against my wishes. As we were transporting her to the ambulance, she hyperventilated herself into syncope.

In the back, I remove the mask to place a Capnoline (like the one in the picture a few posts ago). My partner says to keep her on O2 because "she passed out" (facepalm by me). I tell him that I'll do 4lpm NC, but I just pretend to turn on the O2. Vitals at this time were 114/60, 80P, RR 4, BGL 92, SpO2 100% (room air again haha), ETCO2 of 9. That is what made me think of this call, the ETCO2 of 9. The father was in the back with us, and tells us that his daughter gets panic attacks wen she's ill, because she thinks she's going to die each time (Hx of Sz only, no Sz today). My partner drops a line, and has me do a 12-lead. The 12 is unremarkable.

Meanwhile, the pt had irregular respirations. She was apneic at one point until I shook her. My partner didn't know that I didn't use O2. She started picking up her resps. at the time I got out to drive. She was still dazed, but conscious and following commands a few minutes later at the hospital. I pulled the trends after the call. As her ETCO2 moved up, so did her respiratory rate, which was 16 upon arrival, other vitals largely unchanged. I was comfortable with ruling out a PE as a differential.

The point of all of the above is that I'm wondering if the OP's alcoholic pt also had psych issues. Is it possible that she had a panic attack moments before someone discovered her and called 911?

Low ETCO2 values occur for several reasons. A low flow state, such as profound shock or cardiac arrest can cause low ETCO2, since that reading is dependent on blood returning to the alveoli, to exchange CO2. A PE can block blood flow to a large enough region of a lung to cause a reduced CO2 reading. A pt that is hyperventilating will naturally eliminate a lot of CO2, which puts them into respiratory alkalosis. A pt in DKA, in metabolic acidosis may compensate with hyperventilation, which eliminates CO2 with an effect much like someone having a panic attack, since the underlying problem is metabolic, not respiratory. The increased respirations will not help, just blow off CO2.

When he pt is acidotic, it becomes increasingly difficult for O2 to bind to Hb. Reference the SpO2 dissociation curve, and how rapidly the sat drops after you turn the elbow. When the pt is alkalotic, O2 will readily bind to Hb (Bohr Affect), but the Hb will not release the O2 as readily (basically prevents O2 txp). In addition, you have the cerebral vasoconstriction. So, this is how patients get dizzy and eventually pass out from hyperventilation syndrome.

Since your patient was an alcoholic on some undisclosed meds, is it possible that underlying psych issues caused a hyperventilation episode prior to her being discovered as unconscious by the caller? Probable suicide attempt after all IMO....

 

[Carlos Danger]

But my question is more about physiology I think. Suppose hypothetically that the number was correct. What could be going on in her body to cause this low reading?

Normally, Etc02 closely approximates arterial C02 tensions. So, barring equipment failure, there are only two reasons why the Etc02 would be 9:

• The patient is alkalotic. This means the systemic pH is increased for metabolic or ventilatory (increased minute volume / "hyperventilating") reasons, which results in a corresponding decrease in the Etco2.
  
  Metabolic alkalosis is fairly uncommon, and I think the main toxin in brake fluid is ethylene glycol, which normally causes acidosis rather than alkalosis.
  
  
  
• The patient has an increased C02 gradient as a result of pathology. Normally, since not all the C02 in the blood diffuses across the alveolar-capillary membrane into the alveoli to be exhaled, the Pac02 is 2-5 mmHg greater than the Etc02. This is termed the "Arterial - Etc02 gradient", or P(a-et)Co2. It is analogous to the alveolar-arterial oxygen gradient (A-a gradient).
  
  An increased C02 gradient suggests that Co2 is not making its way from the blood into the alveoli due to low cardiac output, a problem with the alveolar-capillary membrane (pneumonia), ventilation-perfusion mismatch, or possibly some combination of the three (ARDS / ALI).

 

[Handsome Robb]

And after that this thread can end.

Great post! Learn something new every day.

 

[46Young]

And after that this thread can end.

Great post! Learn something new every day.

Not yet!

In my last post, I forgot to add that hyperventilation and the resultant respiratory alkalosis also causes a reduction of available Calcium (hypocalcemia), which can cause tetany, which is where you get the painful carpal-pedal spasm.

That's all I got

 

[MasterIntubator]

...why would her CO2 be only 9?

Did it stay that way, or did it start to rise after 5-10 minutes?

She prob hyperventilated herself out.... takes some time to autoregulate

 

[Simusid]

Did it stay that way, or did it start to rise after 5-10 minutes?

She prob hyperventilated herself out.... takes some time to autoregulate

No she was found unconscious prior to the 911 call, and she remained unconscious throughout the whole transport. That was probably close to 1/2 an hour from the original report. It was an unknown, probably extended downtime. I think the family was worried that they had not heard from her and that is what prompted the call. The two capnography measuerments that I saw were 9 and 8 and they were probably close to 10 min apart.

I know I'm only a basic but I *seriously* doubt this was hyperventilation. I've heard "when you hear hoofbeats, first think horses not zebras" but drinking brake fluid is probably in the zebra category.