# Acid-Base Balance, ABG, iSTAT, EtCO2, and more...



## EMTinNEPA (Sep 12, 2009)

We're covering acid-base balance in school and according to my book (_Paramedic Care: Principles & Practice_) the only way to confirm a patient's pH level is arterial blood gas studies, which are, quote, "only available in the hospital setting".  However, a co-worker of mine mentioned this device...

http://www.rtmagazine.com/issues/articles/2006-04_49.asp

Which is supposedly used in the critical care transport setting for patients who need continuous pH level monitoring.

Has anybody used or seen this device used and how reliable is it?

Also, what's everybody's stance on using EtCO2 as a guidline for determining respiratory acidosis or alkalosis?


----------



## MrBrown (Sep 12, 2009)

Hmm .... I forsee cost outweighting benefit really except in some very sick people being transported inter-facility.  

WRT using EtCO2 for respiratory acidosis or alkadosis IMHO it's really about the same ... it's not a topic I understand well (and I'm not afraid to admit it!) so probably more trouble than it's worth.


----------



## EMTinNEPA (Sep 12, 2009)

A little more on the EtCO2...

According to a medic I spoke with regarding using EtCO2 as an indicator for respiratory acidosis or alkalosis, the EtCO2 measures carbon dioxide exhaled (normal values are 35-45, not sure what the unit of measurement is...).  Since in respiratory acidosis and respiratory alkalosis CO2 is high or low (respectively), wouldn't an EtCO2 of 18 indicate that less CO2 is being retained and the patient is possibly in respiratory alkalosis?

I'm still figuring all this stuff out, so feel free to correct anything that might need correcting.


----------



## Akulahawk (Sep 12, 2009)

To really get an idea of whether or not a patient is acidotic or alkalotic... you'll need to get that ABG done. By measuring only ETCO2, you're only seeing part of the picture. That's just the respiratory side of things. You really do need to measure pH, pCO2, and Bicarb to see whether or not the problem is metabolic/respiratory, compensated, partially compensated, or uncompensated. 

Most of this stuff is from memory... it has been a while since I've seen ABG's...


----------



## VentMedic (Sep 12, 2009)

EMTinNEPA said:


> http://www.rtmagazine.com/issues/articles/2006-04_49.asp
> 
> Which is supposedly used in the critical care transport setting for patients who need continuous pH level monitoring.
> 
> Has anybody used or seen this device used and how reliable is it?


 
Point of Care devices such as the iSTAT have been around for many years (at least 15 years or more) in the hospital and on Flight and Specialty Teams.   In the hospitals, it is not uncommon to see them in the ED, ICUs, OR, Cath Labs or at any patient's bedside for quick analysis.  

They are reliable but cost prohibitive on all ambulances.  As well, few labs are going to extend their licenses to those with little formal education and where QA/QC is of issue.   Few in EMS understand how their glucose montior must be maintained and now you want to introduce something that must be QC'd as frequently as the iSTAT?

As well, the cartridges are very expensive and must be refrigerated until just a few minutes of use.   

Also, what are you going to do the correct.  If you have an acid-base problem that is not clearly respiratory, are you going to use another cartridge for the anion gap to see what type of metabolic acidosis it is.  Then are you going to correct by fluids and if so what type, Tham, NaHCO3 or pressors?  How long are you spending with the patient and how much longer do you want to spend in schoool?



> According to a medic I spoke with regarding using EtCO2 as an indicator for respiratory acidosis or alkalosis, the EtCO2 measures carbon dioxide exhaled (normal values are 35-45, not sure what the unit of measurement is...). Since in respiratory acidosis and respiratory alkalosis CO2 is high or low (respectively), wouldn't an EtCO2 of 18 indicate that less CO2 is being retained and the patient is possibly in respiratory alkalosis?


 
Not necessarily as it all depends on V/Q mismatching, shunting and deadspace ventilation.  This is where the PaCO2 and PeCO2 gradient comes in.  Transport teams check the ABG to determine this gradient because if you muck around with a ventilator thinking the patient is blowing off to much CO2 with mechanical ventilation, you could quickly do great harm to that patient if you try to correct just using a limited understanding of "normal values".     You also wouldn't know if it is alkalosis unless you know the pH.  DKA would be very acidotic but would have a very low CO2.   

The other important aspect of the ETCO2 is understanding the wave forms as that will also tell you a lot about those numbers and you patient but in the field, you should already have formed some idea about what is going on with the patient and use the ETCO2 to confirm your working diagnosis as well as see if there is a change with treatment.


----------



## VentMedic (Sep 12, 2009)

There is one other little matter with doing an ABG.  It is an Arterial Blood Gas from the artery.   Venous blood can work but it depends on the metabolic status of the patient, the pressors and the site the blood is obtained.  If the patient is metabolically unstable or on pressors, I prefer blood from a central line especially if I'm also looking at SvO2.


----------



## Shishkabob (Sep 12, 2009)

MtCAN't always trust EtCO2 for metabolic acidosis.  with cardiac arrest. 

The body is getting acidodic, but EtCO2 will only read 10 if you're lucky, because you're not perfusing enough to get rid if the rest. Therefor it will read respiratory alkalosis, but it won't match up with what the body is doing.





Edit: I lied


----------



## VentMedic (Sep 12, 2009)

Linuss said:


> MtCAN't always trust EtCO2 for metabolic acidosis. Sure, in things like DKA the respiratory acidosis can move in progression to metabolic acidosis, but on the flip side with cardiac arrest.
> 
> The body is getting acidodic, but EtCO2 will only read 10 if you're lucky, because you're not perfusing enough to get rid if the rest. *Therefor it will read respiratory alkalosis,* but it won't match up with what the body is doing.


 
The terms respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic acidosis are dependent on the pH.

For it to be called respiratory alkalosis, the pH would have to be alkalotic. With DKA, the pH is usally still very acidotic regardless of how low the PCO2 gets. You will not normally have a respiratory acidosis with DKA. If you have a combination of both respiratory and metabolic acidosis in a DKA patient, they will be coding or near dead with a pH not compatible with life.


----------



## VentMedic (Sep 12, 2009)

Good sites:

http://fitsweb.uchc.edu/student/selectives/TimurGraham/Welcome.html


http://www.acid-base.com/

http://www.rcsw.org/Download/2006_RCSW_conf/Presentation 2006 RCSW Acid Base Analysis.ppt

http://www.lakesidepress.com/pulmonary/ABG/PREFACEnew.htm

http://classes.kumc.edu/son/nurs466/lecture notes/ABG/ABG 2.htm

Some examples:
http://www.usuhs.mil/med/clerkship/...ources2 Acid baseOptionalslidesetABGcases.ppt

http://www.rtmagazine.com/issues/articles/1999-08_07.asp

http://www.medvarsity.com/vmu1.2/dmr/dmrdata/PEDIA/ABG.htm


----------



## Akulahawk (Sep 12, 2009)

Dagnabbit Vent... stop making me remember this stuff... 

DKA patients can be very acidotic. Just one reason why you see them do Kussmaul respirations is because the body recognizes the acidosis and tries to correct it, and "blowing off" CO2 and ketones is a compensatory effort to raise the pH back towards normal, by creating a "respiratory alkalosis". The ETCO2 of these patients might just be quite low. By maintaining them at a more normal 35-45 mmHg ETCO2 value, you're going to prevent this mechanism from working, and possibly drive the patient even _more_ acidotic... This brings this discussion back around as to why transport teams check the labs, including ABGs.


----------



## MSDeltaFlt (Sep 12, 2009)

EMTinNEPA said:


> We're covering acid-base balance in school and according to my book (_Paramedic Care: Principles & Practice_) the only way to confirm a patient's pH level is arterial blood gas studies, which are, quote, "only available in the hospital setting". However, a co-worker of mine mentioned this device...
> 
> http://www.rtmagazine.com/issues/articles/2006-04_49.asp
> 
> ...


 
I've used iSTAT's and they work fine... limited as Vent says, but fine. I would much rather have the machines close by that can measure everything I need. 

As far as EtCO2's numbers go for respiratory acidosis/alkalosis, it depends on their V/Q, and cardiac output. Also bare in mind that capnography will typically have about a 5-6 torr (their unit of measurement) margin of error under nomal circumstances.



EMTinNEPA said:


> A little more on the EtCO2...
> 
> According to a medic I spoke with regarding using EtCO2 as an indicator for respiratory acidosis or alkalosis, the EtCO2 measures carbon dioxide exhaled (normal values are 35-45, not sure what the unit of measurement is...). Since in respiratory acidosis and respiratory alkalosis CO2 is high or low (respectively), wouldn't an EtCO2 of 18 indicate that less CO2 is being retained and the patient is possibly in respiratory alkalosis?
> 
> I'm still figuring all this stuff out, so feel free to correct anything that might need correcting.


 


VentMedic said:


> Not necessarily as it all depends on V/Q mismatching, shunting and deadspace ventilation. This is where the PaCO2 and PeCO2 gradient comes in. Transport teams check the ABG to determine this gradient because if you muck around with a ventilator thinking the patient is blowing off to much CO2 with mechanical ventilation, you could quickly do great harm to that patient if you try to correct just using a limited understanding of "normal values". You also wouldn't know if it is alkalosis unless you know the pH. DKA would be very acidotic but would have a very low CO2.
> 
> The other important aspect of the ETCO2 is understanding the wave forms as that will also tell you a lot about those numbers and you patient but in the field, you should already have formed some idea about what is going on with the patient and use the ETCO2 to confirm your working diagnosis as well as see if there is a change with treatment.


 
And one other thing. Charles' Law still works in blood relating to ABG's. What I mean is gases will still expand or contract relative to temperature. ABG's default to 98.6F on analysis. It's been my experience not to see much difference in 1 or 2 degree changes. However, if your pt is febrile (101F or higher generally speaking), then your PaO2 will be higher making your SaO2/SpO2 read higher and PaCO2 will be higher moving your pH down some.

The opposite will happen if your pt is markedly hypothermic. PaO2 and SAT's will be lower, and your PaCo2 will be lower making your pH ligher.

You should also keep this in the back of your mind. What is their normal temp? I've seen several little old ladies and some young girls run 96.9-97.3F temp and that is their normal.

Vent please check my stats, but that's my take on it.


----------



## VentMedic (Sep 12, 2009)

Mike's comments now bring us to the oxyhemoglobin dissociation curve.  This is another important set of details that anyone who touches a pulse oximeter should at least be aware of even if you don't know what an ABG is.


----------



## daedalus (Sep 12, 2009)

VentMedic said:


> Mike's comments now bring us to the oxyhemoglobin dissociation curve.  This is another important set of details that anyone who touches a pulse oximeter should at least be aware of even if you don't know what an ABG is.



My limited understanding of the curve is that when the oximeter reads 90-100, you have a pretty stable PaO2, and that after the oximeter starts to go down from 90, you lose PaO2 precipitously.


----------



## MSDeltaFlt (Sep 12, 2009)

VentMedic said:


> Mike's comments now bring us to the oxyhemoglobin dissociation curve. This is another important set of details that anyone who touches a pulse oximeter should at least be aware of even if you don't know what an ABG is.


 
If this is considered a hijack, please let me know and I'll just PM.

Loosely translated: if your pt is markedly febrile, as in septic, then their oxyhemoglobin dissociation curve will shift to the right meaning their blood will have an increased affinity for oxygen.  Meaning it's going to really like oxygen and not want to let any of it go (to the tissues).  Ever notice those in septic shock are on a butt load of O2?  This would be one reason why.


----------



## ResTech (Sep 12, 2009)

> The body is getting acidodic, but EtCO2 will only read 10 if you're lucky, because you're not perfusing enough to get rid if the rest. Therefor it will read respiratory alkalosis, but it won't match up with what the body is doing.



EtCO2 measures ventilatory status when perfusion is normal. When perfusion is decreased (ie cardiac/resp arrest, cardiogenic shock, trauma) EtCO2 measures perfusion. 

When cardiac output is decreased, pulmonary blood flow is also decreased which limits the amount of CO2 being delivered to the lungs and thus being exhaled which is gonna display as a low EtCO2 value even though the blood is acidotic. 

It's also my understanding that with decreased cardiac output there is obviously less oxygen distribution which decreases cellular metabolism which causes less CO2 to be produced. Instead, other acids like pyruvic acid from the first stage of the Krebs cycle is produced which then converts to lactic acid when perfusion is not restored leading to the acidosis.

I have been trying hard to keep this all straight so hopefully I got it right... ha ha... if not please clarify. 

Here is an image to show how cardiac output correlates to EtCO2:


----------



## MSDeltaFlt (Sep 12, 2009)

ResTech said:


> EtCO2 measures ventilatory status when perfusion is normal. When perfusion is decreased (ie cardiac/resp arrest, cardiogenic shock, trauma) EtCO2 measures perfusion.
> 
> When cardiac output is decreased, pulmonary blood flow is also decreased which limits the amount of CO2 being delivered to the lungs and thus being exhaled which is gonna display as a low EtCO2 value even though the blood is acidotic.
> 
> ...


 
Kind of.  There is no switch that gets flipped from measuring ventilatory status to measuring perfusion.  EtCO2 measures exhaled CO2.  That's it.  Nothing else.  However it does require adequate cardiac output in order to read exhaled CO2 within the accepted 5-6torr margin of error that we need.  It also needs HCO3 levels to be adequate as well.

Metabolic acidosis will also render EtCO2 to read low even when HR & BP remain unchanged.

Capnography requires more interpretation than some may realize.


----------



## ResTech (Sep 12, 2009)

Here are a few excerpts on EtCO2 in relation to cardiac output... all from capnography.com



> Reduction in cardiac output and pulmonary blood flow result in a decrease in PETCO2 and an increase in (a-ET)PC02.1,2 The percent decrease in PETCO2 directly correlated with the percent decrease in cardiac output (slope= 0.33, r2=0.82 in 24 patients undergoing aortic aneurysm surgery with constant ventilation).3 Also, the percent decrease in CO2 elimination correlated with the percent decrease in cardiac output similarly (slope=0.33, r2=0.84).3 The changes in PETCTO2 and CO2 elimination following hemodynamic perturbation were parallel. These findings suggest that decrease in PETCO2 quantitatively reflect the decreases in CO2 elimination.3





> Increases in cardiac output and pulmonary blood flow result in better perfusion of the alveoli and a rise in PETCO2





> A PETCO2 greater than 30 mm Hg was invariably associated with a cardiac output more than 4 L/min or a cardiac index > 2 L/min.4 Furthermore, when PETCO2 exceeded 34 mm Hg, pulmonary blood flow was more than 5 L/min (CI > 2.5 L).4





> Thus, under conditions of constant lung ventilation, PETCO2 monitoring can be used as a monitor of pulmonary blood flow.4-8





> Callaham M et al (10) used initial PetCO2 readings to predict return of spontaneous pulse during CPR. Patients who developed a pulse had a mean PetCO2 of 19 +/- 14 Torr at the start of resuscitation and those who did not had a mean PetCO2 of 5 +/- 4 Torr. Using an initial PetCO2 value of 15 torr identified 71% of the patients who were subsequently resuscitated with a specificity of 98%. PetCO2 value is not a sufficient criterion by itself for terminating resuscitation efforts.


----------

