Is PEtCO2 Overrated?

A

Aprz

The New Beach Medic
Messages
3,035
Reaction score
666
Points
113
For the past couple of months, maybe year, I've been hearing paramedics and instructors talk about the latest big thing, PEtCO2 (end tidal carbon dioxide, often referred to as "capnography" or "end tidal"), and how it's really good, and way better than SpO2 (pulse oximetry or "pulse ox"). They talk about using it for everything from monitoring the effectiveness of chest compressions and probability of resuscitating a patient in cardiac arrest to patients experiencing diabetic ketoacidosis (DKA).

I remember reading Avoiding Common Prehospital Errors, and one of the first few chapters talks about how great PEtCO2 is.

I think it's good for detecting bronchospasms via the capnography waveforms if it's got shark fin waveforms.

wave-5.jpg


I think it's good for detecting whether you've successfully done tracheal intubation, or successfully done a esophageal intubation (whatever you consider success), and monitoring that the endotracheal tube remains in the trachea while moving, transporting, or doing chest compressions on a patient.

As explained before, it's great for detecting the effectiveness of chest compressions, and if you're sure that your chest compressions are good (deep and fast, correct placement), that it's a good indicator of the likeness of the patient being resuscitated (less than PEtCO2 10 mm Hg indicates poor chest compressions or the patient is unlikely to be successfully resuscitated). It can also be used as a replacement of pulse checking, just look for a sudden rise in PEtCO2.

There are other things that I don't feel like it's as great for, but I hear it brought up all the time. For example, DKA. I think in cases like DKA, PEtCO2 is only good for showing that the patient is either hyperventilating or hypoventilating. It's really just an alternative to counting the respiratory rate. The patient is breathing faster so they are getting rid of more carbon dioxide (CO2), and therefore their PEtCO2 should be low (for DKA, or any other condition that causes hyperventilation), or the patient is breathing too slow and/or too shallow so they are not breathing off CO2 as quickly, and therefore their PEtCO2 is higher than normal. To me, it seems like a blood glucose level (BGL) would be a way better indicator of DKA than PEtCO2. What about other causes of hyperventilation like salicylate overdose? Why is DKA brought up in PEtCO2 discussions frequently?

Click here to see a study done on PEtCO2 and pediatrics with DKA.

Capnography just doesn't seem as amazing as people make it sound to me. I'm starting to see it more frequently used on a variety of patients, but often it provides no significantly clinical or diagnostic information.

I was wondering if maybe PEtCO2 is starting to be just as overrated, and maybe blindly done like some other diagnostics like BGL, SpO2, 3-lead electrocardiography (ECG) monitoring, 12-lead ECGs, etc.? If it may become as overrated as supplemental oxygen.

I also think how it's interesting and funny that paramedics and instructors seem to love PEtCO2, but say "treat the patient, not the monitor" when it comes to ECG interpretations.

My opinion is it's just another tool like pulse oximetry, and it shouldn't be used blindly on every patient. For patients that are hyperventilating or hypoventilating, I may use it as another objective finding to demonstrate on my chart or care report that the patient is hyperventilating or hypoventilating. I fear that it is becoming highly overrated.

What do you guys think?

Some links on capnography:
http://www.paramedicine.com/pmc/End_Tidal_CO2.html
http://www.capnography.com/new/
 
Last edited by a moderator:
I think the use of EtCO2 for acidotic states, and DKA, in particular is an inexact art and one we're working on. It's really never going to be as accurate or useful as an ABG or proper lab values, but in the field it's something we can use to help guide our thought processes and provide additional info. when we're already leaning one way. You're absolutely right in saying BGL and clinical presentation is far more important in suspecting and treating DKA than EtCO2 values.

As far as utility goes, I think it adds significant value to titrating proper ventilatory rates and measuring the effectiveness of respiratory therapies. Don't look at it as following the cheap cliche of "treat the patient, not the monitor." Just like EKGs, capnography can be an incredibly useful tool and one that can show useful information that would otherwise not be easily gleaned prehospitally. Also similarly to EKGs, over reliance on this single tool over others can lead to tunnel vision and poor care.
 
It's really the only quantitative tool we have to assess ventilatory status, and it should be used in conjunction with other diagnostic tools to help give a more well rounded snapshot of a patient's condition. It's not the end all, be all... but it is a useful tool and NOT overrated, unless you're basing treatment solely on an ETCO2 waveform and capnometery.
 
I think I'm on the same page... Great for confirming tube placement, checking quality of compressions and can indicate ROSC, but otherwise it's just clutter. Do I really need to use the waveform to diagnose bronchospasm? Well, if the dyspnea, wheezing, prolonged expiratory phase and guy waving at you and saying "I have asthma" aren't enough...
 
TheLocalMedic said:
Do I really need to use the waveform to diagnose bronchospasm? Well, if the dyspnea, wheezing, prolonged expiratory phase and guy waving at you and saying "I have asthma" aren't enough...
Click to expand...

Exactly.

Aprz said:
I was wondering if maybe PEtCO2 is starting to be just as overrated, and maybe blindly done like some other diagnostics like BGL, SpO2, 3-lead electrocardiography (ECG) monitoring, 12-lead ECGs, etc.? If it may become as overrated as supplemental oxygen.

I also think how it's interesting and funny that paramedics and instructors seem to love PEtCO2, but say "treat the patient, not the monitor" when it comes to ECG interpretations.

My opinion is it's just another tool like pulse oximetry, and it shouldn't be used blindly on every patient. For patients that are hyperventilating or hypoventilating, I may use it as another objective finding to demonstrate on my chart or care report that the patient is hyperventilating or hypoventilating. I fear that it is becoming highly overrated.

What do you guys think?
Click to expand...

I agree with you 100%

When 12-leads started to become common in the field years ago, no one had any idea how to use them but were sure that they were going to revolutionize prehospital care. I'd say they do some good things for sure - STEMI activation by prehospital EKG has undoubtedly saved some lives - but the initial excitement was way overblown.

You see the same thing now with capnography, except that capnography is harder to interpret because of all the factors that can affect it, and is not going to activate any "code" response at the hospital like an EKG can. It is really useful only as a trending tool, which severely limits its utility in short (most) transports. It generally reveals a ventilatory problem, which will be clinically evident if it is severe enough to require prehospital treatment, or possibly a metabolic problem, which can't be treated prehospital.

Would anyone treat an Etc02 value or capnograph, if no clinical signs correlated? I hope not. So what then is the value of Etco2?

Just like Sp02, I think it is worth having, because it is cheap per patient and does reveal some objective data that may prove useful in some limited situations. But I think the utility of any monitoring modality should be judged on how it affects treatment and eventual outcomes. And aside from confirming ETT placement, I just don't see capnography affecting treatment in EMS.
 
Last edited by a moderator:
The thing about capnography, 12-lead assessment, and 12-lead monitoring is this. Vendication. Vendication proving your prehospital care plan was accurate. And also vendicating your NOT treating certain manifestations should your assessment contradict the patient's complaint.
 
One of my hobbies is building stuff... I have lots of tools in my workshop, LOTS of tools. When I tinker with stuff I use the tools I need to get the job done. I don't use stuff just to be using it, nor do I use tools for what they were not designed for. Which tool to use comes from years of practice and of course my judgment. I would not expect a non-craftsman to come into my workshop and turn out the same work as I do

In EMS (and non-EMS) medicine we have lots of tools to use also. We need to use them in the same manner as I use the tools in my workshop. If I want a basic SPO2 on a patient I pop on a pulse ox, if I want to see their ventilatory status "breath by breath" I'll pop on an end tidal, if I want to see what the heart rhythm is I'll use the 4 lead, if I I need more info I'll up it to 12. Same with BGL, or lactate, or any other POC lab work, do I need the number, will it be important to my differential or treatment?

I guess what I'm getting at in a long winded way is that we have a bunch of tools we can use. How we use them, and why is our choice. Tools add to our clinical judgment and make our job easier, or as MSDelta said, validates our clinical course with tangible numbers.

Use your tools when you need them and remember that tools without a craftsman are just expensive paperweights!
 
Pavehawk, that was probably one of the best analogies I've ever read, very well written. And you're right, all tools have an appropriate use. However, with pre-hospital medicine I just don't see capnometry/capnography being used as often as it is touted that it can be.
 
I'd say that the "shark fin" wave form assoc'd with asthma is over-rated. Seen only a few times despite all the COPD and asthmatics whose EtCO2 I monitored. Never once saw it when I didn't already know they were experiencing constriction.
 
In addition to the aforementioned uses, I like ETCO2 for an additional measure of capture with external pacing (more perfusing beats = rising BP = rising ETCO2), and an early indicator of falling blood pressure. It's also useful in helping to decide (along with a comprehensive assessment, of course) if you need to ventilate a Sz pt, or an opiate OD with hypoventilation, vs just a NC or NRB.
 
Yeah, I was a bit disillusioned when I started looking into exactly what info one can get from capnography... I thought it would be more impressive.

Having said that, using it as a guide for chest compressions, knowing when to even do a pulse check (if your agency allows you to deviate from AHA ACLS), and recognizing esophageal intubations, it's outstanding. The later one is something that shouldn't really be a big problem, but it really really is when you add up all the UNDETECTED esophageal intubations or tube displacements...

So, I'm glad it's being treated as the next best thing...even if it's the next best thing only because it's preventing preventable mistakes...at least it's saving some lives out there.


As far as 12-Leads, I've heard some promising information about its future in medicine. Things from diagnosing pulmonary emoblisms, to increased ICP, to shock (I THINK I'm getting those three right)...at least according to some of the advance 12-lead whizzes
 
For pulmonary embolism, I've read it's a rare finding (like low 20%). Most common ECG finding for pulmonary embolism is tachycardia. Also people know of an S-wave in lead I, Q-wave in lead III, and inversed T-wave in lead III also (a.k.a S1Q3T3), which is a right ventricular strain pattern (so you can see it in other conditions that causes the right ventricular strain eg shortness of breath). Another right ventricular strain pattern I believe is down sloping for the ST segment with depression (it goes down at a 45 degree angle, it's not flat at like a 90 degree angle). Another finding of a pulmonary embolism is a pseudo/incomplete right bundle branch block (RBBB) which has all the features of an RBBB (rsR' or qR in lead V1, "slurred" S-wave in lead I and V6, pretty much Rs in lead I and V6) , but the complex is less than 0.11s in width, and lead V1 might not be mostly positive (R/S <1) like a normal RBBB. You might see a inversed T-wave in all of the inferior leads (II, aVF, and III) and/or the anteroseptal leads (V1-V4). You may see ST depression in the anteroseptal leads also.

In cerebral hemorrhage, it'll sometimes have deep inversed symmetrical T-waves I've read. I do not know if it's from increased intracranial pressure (ICP) and if it's seen in cerebral ischemia. I do not understand this finding.

I haven't heard of any unique findings for shock.

I think it's interesting that people find capnography very useful for diabetic ketoacidosis (DKA), but probably wouldn't do a 12-lead on a patient with DKA.
 
You must log in or register to reply here.
Back
Top