End Tidal in self ventilating patients

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Radley

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Hi, I'm wondering if anyone out there uses end tidal capnography in the form of nasal specs (or anything else) to monitor ETCO2 in non-intubated self ventilating patients?? I'm from Australia and doing a research proposal to potentially have this introduced for monitoring ventilations of our patients in restraints and vac mats whilst sedated or analgesed.

Would welcome any ideas/feedback on anyone's current use of this technology

Cheers
 
We have them for our LP15's at work and I love them!

I use them for objective measure of respiratory rate, for confirmation of bronchoconstriction and as a monitor for alkalosis/alkalosis. I apply them to all my SOB patients, overdoses and decreased LOC's.

They're a great little tool to add to your assessment and monitoring.
 
We use them a lot. Any respiratory, and pain med/sedation, and any priority 1 call for baseline etco2.
 
I use them on almost every respiratory call. I find it to be much more reliable and more indicative of how well a Pt is moving air than spo2. I do use both in conjunction but would be just find with the etco2.

I like seeing the waveform on the monitor to verify bronchoconstriction as well.

Also, not having to use your watch to get a respiratory rate saves a little time as well.

I also like to turn the monitor into a game for anxiety patients. I tell them that the goal is the slow their breathing down enough that the number on the screen reaches 35 haha.
 
Actually, a question about this... Are you able to tie an ETT adapter on to a bousgniac or other disposable CPAP setup, or does it cause too much of a leak in the system? Does the nasal adapter fit, or cause a mask seal? Is there a better way to watch ETCO2 for CHFers?
 
I place an end tidal nasal cannula under the CPAP mask. According to the Oridian folks, you can't use an ET tube filter set on anything other than an ET. There is too much dead space in a mask to get a reliable reading.
 
Thanks for your feedback guys/girls. Just wondering do any of you have any evidence that has been peer reviewed showing nasal canulla end tidal in the pre hospital setting?? It's pretty tough to find...or non existent!!
 
I do not know of any service in Australia that uses this, certainly in New Zealand we do not and have no plans to introduce it, I am also not aware of any evidence that shows it is beneficial.

I do not think the cost is justified myself; it won't really change what you do to the patient in the vast majority of incidences and is a "nice to have" not a "have to have".

For those patients where maintaining normal level of CO2 in the blood is important e.g. post cardiac arrest or traumatic brain injury who are intubated and ventilated we already have main stream ETCO2.
 
I disagree. I believe end-tidal capnography is the only real way to quantitatively measure of ventilation in a self ventilating patient. With trending of capnometry and the capnography waveform, you can get a great picture of the ongoing ventilatory status of bronchial constricted patients. We also use end-tidal to help guide treatment with patients that are on CPAP, receiving inhaled beta agonists and sedation.

I've seen studies on using sidestream end-tidal to guide treatment, like CHF vs COPD. I'll see if I can hunt some of that stuff down. I know that all of the studies measuring end-tidal CO2 versus arterial blood gas have shown them to correlate very closely with the arterial CO2.

Utilizing sidestream capnography in self ventilating patients is fast becoming a standard of care in many EMS agencies. I wouldn't be surprised if everybody is doing this within the next few years.
 
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Interesting.

Isn't oxygenation the primary concern? I am not really worried how a patient is ventilating as liong as they are oxygenation is sufficient; obviously if somebody is tachypnoea'ing along at 100 breaths a minute why are they doing so? I would bet my next paycheck (and I need it!) on the fact they are hypoxaemic!

How exactly does side stream CO2 change what you do to patients who receive salbutamol or sedation? I have been taught to give salbutamol as required to patients with mild to moderate asthma or give as continuous if severe/ life threatening. Asthma patients will be hypercapnoeaic and should be allowed to remain permissively high.

Sedation is an ICP thing so not my expertise but I believe oxygen via nasal prongs is standard for somebody who is getting sedated.
 
I suggest doing a little bit a reading on capnography.

http://emscapnography.blogspot.com/?m=1

10 things every paramedic should know about capnography is a great read.

And I don't really care about oxygenation, I care much more about ventilation. I want to make sure that the gas exchange is happening as it needs to. One great example is watching a tight, constricted shark fin capnography waveform become a flat expiratory plateau with the administration of nebulized beta agonists. It's also a great way to be able to tell if your patient who suffers CHF and COPD has bronchial constriction and may require some albuterol to open things up along with CPAP. In patients receiving sedation, you can closely monitor their respiratory drive by watching the trending and having a visual indicator with the capnography waveform.

If your monitor can measure end-tidal CO2 for endotracheal tube placement, there is no reason to not carry a sidestream capnography device.
 
There is truck loads of evidence to suggest pulse oximetry is a lagging indicator- and is not an appropriate guide to ventilation. Ventilation and oxygenation are very different beasts. study's have shown patients saturating at 94% with an end tidal of 100mmhg who have had significant periods of apnea only noticed once the patient has become unrousable. One paper I read shows patients monitored with nasal canulla end tidal were 17 times more likely to have reduced ventilation noted by staff before those pts being monitored by spo2 alone... I'm certainly on the "for" side. It's appears best practice and I'd expect it to become the norm sooner rather than later
 
Clare said:
Interesting.

Isn't oxygenation the primary concern? I am not really worried how a patient is ventilating as liong as they are oxygenation is sufficient; obviously if somebody is tachypnoea'ing along at 100 breaths a minute why are they doing so? I would bet my next paycheck (and I need it!) on the fact they are hypoxaemic!

How exactly does side stream CO2 change what you do to patients who receive salbutamol or sedation? I have been taught to give salbutamol as required to patients with mild to moderate asthma or give as continuous if severe/ life threatening. Asthma patients will be hypercapnoeaic and should be allowed to remain permissively high.

Sedation is an ICP thing so not my expertise but I believe oxygen via nasal prongs is standard for somebody who is getting sedated.
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A few examples of times when etco2 leads me when accompanied by a complete assessment:

Chronic COPDer who calls regularly when the nebs aren't helping him- etco2 shows bronchi constriction vs chf or pneumonia. It's right there in the shark fins.

Massive narcotic overdose in which the 4 MG of Narcan I have on the truck need to last an hour to the hospital. That gives me 10 0.4 MG doses to titrate to respiratory status. RR<12, another dose.

Trauma pt in which I want to know immediately when air exchange drops off because of the pneumo? Watch the height of the waveform. It's breath-by-breath analysis.

Swirling the drain unconscious septic person with a gag reflex lacking peripheral perfusion to make the pulse ox work? I know when they lose their pulse.

And so on. It's fun to have on DKAs and metabolic problems that you can infer the acid-base numbers- or play at it, but that really is just nice to have.

Actually, it isn't- 18 yo DM1 and asthma complaining of breathing difficulty will show you in 2 seconds that she's in DKA and has no bronchoconstriction.
 
The times I found EtCo2 to be most helpful (for non intubated patients, that is), was for assessing gas exchange in dyspneic patients or in altered mental status. A few times I had patients with decent vitals (w/ AMS) who were found to have EtCO2 be 80s to even 100+. I can even think of a few times a nasal EtCO2 would have helped in hospital (had a patient on the floor with a h/o pickwickian syndrome who became altered... ABG showed a pCO2 of 90 something.)

While the slurred upstroke might be helpful for identifying bronchoconstriction, I question how sensitive it is. I don't think there is enough evidence to support treating the waveform alone or basing a treatment on the waveform (I'd be more concerned about the value). If you're looking to EtCO2 to help differentiate COPD from CHF, you're going to be disapointed. I've had plenty of patients with wheezing who did not have a remarkably sloped waveform, even the ones who initially had quiet chests who became loud wheezers with albuterol. Often, those patients had high EtCO2, which I found to be more concerning.
 
Obviously, using only end-tidal CO2 to differentiate COPD from CHF is a fool's errand. However, a sharply sloped end-tidal waveform is indicative of bronchoconstriction. I'm not mistaken, CO2 diffuses through fluid as it does through air, so there would be no trapping of the CO2 which would lead to a slurred expiratory plateau. When I see a patient in respiratory distress and my end-tidal waveform displays sharply defined shark fins, I treat that with bronchodilators. Of course, I seem to be using CPAP in conjunction with nebulized albuterol and ipratropium a lot more these days.
 
n7lxi said:
Obviously, using only end-tidal CO2 to differentiate COPD from CHF is a fool's errand. However, a sharply sloped end-tidal waveform is indicative of bronchoconstriction. I'm not mistaken, CO2 diffuses through fluid as it does through air, so there would be no trapping of the CO2 which would lead to a slurred expiratory plateau. When I see a patient in respiratory distress and my end-tidal waveform displays sharply defined shark fins, I treat that with bronchodilators. Of course, I seem to be using CPAP in conjunction with nebulized albuterol and ipratropium a lot more these days.
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But, how often is the "shark fin" wave form the only indicator of bronchoconstriction? Usually there are physical signs - actual wheezing or diminished breath sounds w/ increased work of breathing. As far as CHF, the diffusion coefficient of CO2 in water is 10,000 times less than air. But, that would, I think, add to a great a-A gradient. The problem with CHF is the concomitant bronchoconstriction that can occur, even in the absence of a comorbid obstructive disease. The presence or not of a shark-fin waveform may not have any bearing on whether the patient is in COPD or CHF. As far as I know, there is no study of the waveform and its PPV or NPV for CHF or COPD. As of now, I don't really think of it as a diagnostic tool, but an adjunct. Basically, I think the shark-fin waveform is overhyped as we do not know just how useful it is.
 
n7lxi said:
Sounds like it's time for a study…
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I'm probably going to take a month next year to do some dedicated EM or EMS-related research. This has been on the back of my mind as a potential subject, but there are a lot of topics I'd like to address... and, there is only so much that can be done in a month.
 
Clare said:
How exactly does side stream CO2 change what you do to patients who receive salbutamol or sedation? I have been taught to give salbutamol as required to patients with mild to moderate asthma or give as continuous if severe/ life threatening. Asthma patients will be hypercapnoeaic and should be allowed to remain permissively high.
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I'm still finding my own comfort level with the ETCO2 on spontaneously ventilating patients. That being said:

Asthma: I think it serves as part of the overall gestalt. If you have "sharkfinning", and it improves following therapy, it's a sign of improvement. Obviously this has to be interpreted in context of the patients accessory muscle use, lung sounds, dyspnea, oximetry, mentation, etc. A normal or high ETCO2 in an asthmatic suggests that the patient is fairly sick. Most mild cases present with respiratory alkalosis and a low PETCO2.

Sedation: The issue with sedation is that you can have hypoventilation and begin retaining CO2, leading to CO2 narcosis which can ultimately cause coma, cardiac arrhythmia, etc., while showing normal oximetry. Most of the patients that I sedate, I'm not trying to put that deep. However a lot of the patients I encounter have performed their own conscious sedation, and the ETCO2 serves as another consideration as to whether I need advanced airway, or should consider narcan. If they're breathing 10/min, but have an ETCO2 of 60mmHg, and no prior COPD history, then they need assisted ventilation.


Sedation is an ICP thing so not my expertise but I believe oxygen via nasal prongs is standard for somebody who is getting sedated.
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Not sure I follow what you're saying here. I'm more concerned about ICP management in my intubated head injuries. Personally, I don't give oxygen to everyone I'm sedating, and even if I do, all this does is ensure that if they hypoventilate their CO2 levels can rise higher before their SpO2 starts falling.

Prehospitally you're usually giving 1:1 care, so I think some of the real value here would be on an post-surgical recovery ward, or in the ER following procedural sedation, if you're not always going to have someone bedside.

I could work quite comfortably without the ETCO2 nasal cannula. However, I'm lucky enough to have access to it, so I try and use the information to the best of my abilities.
 
systemet said:
Not sure I follow what you're saying here. I'm more concerned about ICP management in my intubated head injuries. Personally, I don't give oxygen to everyone I'm sedating, and even if I do, all this does is ensure that if they hypoventilate their CO2 levels can rise higher before their SpO2 starts falling.
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She is from NZ, and there, sedation is an Intensive Care Paramedic (ICP) skill.

Typical abbreviation confusion.
 
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