Cardiac Arrest Acidosis and ETCO2

[Swatseal]

New member, I searched through related posts and couldn't find anything that answered this question. I'm a new medic (couple months), and I was discussing with another medic the use of sodium bicarb in arrest patients and some indicators that it should be given. I thought I understood ETCO2, but now I am confused. Both scenarios assuming proper CPR, medication administration, defibrillations, and fluid administration.

Scenario 1: Ventilation quality is good, with a rate of 10-12, and good compression rate and quality during cardiac arrest. In this case, if the ETCO2 is below 20 mmHg, would that not be an indicator of metabolic acidosis and indication of sodium bicarb administration. The bicarb would buffer the hydrogen ions and help increase the CO2.

Scenario 2: Another medic was telling me about a CODE where a suspected saddle PE was involved (line of demarcation across the chest). He said they successfully got ROSC and ETCO2 remained in the 80s. He stated ETCO2 spiked into the 90s during ROSC, but that it was in the 80s prior to ROSC. He stated when they got to the hospital, the Dr asked why they had not given bicarb to this patient.

This is where I am getting confused. In awake patients, ETCO2 below 25 mmHg (assuming adequate ventilation rate and quality) would indicate poor perfusion or metabolic acidosis...just like it does in scenario 1. I think I understand the low ETCO2 in the first scenario and how sodium bicarb assists with the metabolic acidosis. I don't understand how the high ETCO2 considering the ventilation quality and rate combined with the compression rate and quality would indicate sodium bicarb administration.

If someone could explain this to me I would greatly appreciate it.

 

[Aidey]

You've got something backwards.

An EtCO2 under 35mm/hg indicates alkalosis. An EtCO2 above 45mm/hg indicates acidosis.*

So the quick answer to scenario 1 is that you're over ventilating or the patient is moving from mostly dead to all dead, bicarb would make the situation worse. The quick answer to scenario 2 is that bicarb was probably indicated assuming the pt was being ventilated at an adequate rate/depth and with 100% oxygen. Reducing the EtCo2 can help prevent re-arrest by helping the acidosis. In many patients once ROSC is achieved this can be done through ventilation alone, but bibarb can be helpful sometimes.

*This is the simple explanation. Someone with metabolic acidosis can have a low EtCO2 because they are hyperventilating in an attempt to 'blow off' the excess CO2. A common example of this is DKA patients. I've seen them have EtCO2 levels below 10mm/hg before.

 

[Sublime]

I think you're confusing PH with ETCO2 as far as how they're calculated. Lower PH = More Acidic. Lower ETCO2 = More Basic

http://emtlife.com/showthread.php?t=28055

Go to the link above for a great thread with a lot of info on Bicarb admin.

 

[usalsfyre]

Scenario two makes zero sense to give bicarbonate as well because if you can't adequately perfuse lung tissue to get rid of the CO2(like in a saddle embolus) your only going to make the acidosis worse.

Must have been an old school doc.

 

[Swatseal]

Thank you guys for the replies. I will read up on the post you linked. Here is a recent article I read where it talks about administering bicarb in arrest patients with low ETCO2 and proper ventilation and perfusion:

Because CO2 is a by-product of metabolism, anything affecting the metabolic rate affects CO2 production and, consequently, corresponding end-tidal carbon dioxide (EtCO2) levels. Metabolic pathways must be supplied with essential nutrients, such as sugar, water and oxygen for a normal metabolic rate to occur. So if perfusion is compromised, so is the delivery of these components necessary for metabolism. The result is a decreased metabolic rate, resulting in decreased CO2 production. Or, if a patient is in metabolic acidosis (clinically defined as an acidotic pH with depleted bicarbonate), less CO2 will be created, resulting in lower EtCO2 levels.

Here is the link to the full article: jems.com/article/patient-care/capnography-use-optimizes-ems-perfusion (sorry, can't link yet). Is this talking about something different, or how does it relate?

 

[KellyBracket]

We use the PETPCO2 for different things at different times - it means different things in COPD, in asthma, and especially in cardiac arrest.

When a patient is first intubated, you just want to see a non-zero number.

After ROSC, you adjust ventilations to keep the PETCO2 around 35-40. There's no need to get fancy, unless some specific tox-metabolic circumstance dictates.

During CPR, it mostly tell you about cardiac output. From the AHA ACLS guidelines:

"If Petco2 is <10 mm Hg, it is reasonable to consider trying to improve CPR quality by optimizing chest compression parameters (Class IIb, LOE C).
If Petco2 abruptly increases to a normal value (35 to 40 mm Hg), it is reasonable to consider that this is an indicator of ROSC (Class IIa, LOE B)."

In any case, leave the bicarb in its box. The evidence that it does any good during undifferentiated cardiac arrest is really weak.

 

[KellyBracket]

Thank you guys for the replies. I will read up on the post you linked. Here is a recent article I read where it talks about administering bicarb in arrest patients with low ETCO2 and proper ventilation and perfusion: ...
Here is the link to the full article: jems.com/article/patient-care/capnography-use-optimizes-ems-perfusion (sorry, can't link yet). Is this talking about something different, or how does it relate?

I don't believe the author was describing administering bicarb, but rather the state of the body's own bicarb supply.

 

[Swatseal]

I don't believe the author was describing administering bicarb, but rather the state of the body's own bicarb supply.

The author may not talk about administering bicarb in the article, but I know that is what he is getting at. He taught our capnography section during paramedic school. He also wrote a book called "Capnography: King of the ABCs," which is a great read. His book didn't mention anything about abnormally high ETCO2 after ROSC, which is why I asked the question. Here is a small exert from pg 55 of the book:

Administering bicarbonate to a patient in acidosis, such as in cardiac arrest, would cause a rise in the patient's pCO2 translated to an increased ETCO2, assuming that compression and ventilatory rates remain unchanged. Generally, increases in ETCO2 levels from bicarbonate administration are shorter in duration than ETCO2 increases seen with return of spontaneous circulation (ROSC) (see ROSC section).

Bicarbonate administration should be considered if ETCO2 levels begin to decrease in the presence of good CPR and an appropriate ventilatory rate. If paramedics approach bicarbonate administration from a "cookbook" approach (going through the algorithms with minimal critical thinking), potentially more harm than good can be done as extreme alkalosis is just as detrimental to a patient as extreme acidosis.

He goes on to talk about "titrating" bicarb to effect base off of your ETCO2 instead of administering entire amps or 1 mEq/kg.

What I am not understanding is he says low ETCO2 can be indicative or metabolic acidosis, yet that doctor in the OP and many others state high ETCO2 can indicate metabolic acidosis. I'm just not understanding how values on opposite ends of the spectrum can represent the same thing.

 

[MSDeltaFlt]

The author may not talk about administering bicarb in the article, but I know that is what he is getting at. He taught our capnography section during paramedic school. He also wrote a book called "Capnography: King of the ABCs," which is a great read. His book didn't mention anything about abnormally high ETCO2 after ROSC, which is why I asked the question. Here is a small exert from pg 55 of the book:



He goes on to talk about "titrating" bicarb to effect base off of your ETCO2 instead of administering entire amps or 1 mEq/kg.

What I am not understanding is he says low ETCO2 can be indicative or metabolic acidosis, yet that doctor in the OP and many others state high ETCO2 can indicate metabolic acidosis. I'm just not understanding how values on opposite ends of the spectrum can represent the same thing.

I understand what you're confused about here. When you were asking how, after ROSC, low ETCO2 could mean a low pH it would be because of decreased cardiac output. I.e. low BP/HR. You'll be able to tell your pt is about to lose pulses again just by looking at EtCO2.

Now in scenario 2 would be completely different. When it comes to ABG's (pH, PaCO2, PaO2), think of it this way: R.O.M.E. Respiratory Opposite, Metabolic, Equal.

When PaCO2 goes up, Ph goes down and vise versa considering normal cardiac output. And also when HCO3 foes up, pH goes up and vise versa (seen in pts with DKA).

You see a pt in ROSC will become acidic because metabolism continues even after pulses stop. Lactic acid is still being made. And when a pulse is returned the blood begins to circulate all that lactic acid around making the blood more acidic bringing down the pH.

But that's another story we can delve into later

 

[KellyBracket]

He goes on to talk about "titrating" bicarb to effect base off of your ETCO2 instead of administering entire amps or 1 mEq/kg.

Does he provide citations to any studies that used bicarb during CPR in this "titration" manner? I'd love to check them out.