Any EM residents / Attending care to weigh in on ETCO2 and ACLS Q

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EmergDoc2B

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Does administration of bicarb during ACLS throw off the recommended ranges of ETCO2 when assessing adequate chest compressions? In theory The CO2 levels should increase as bicarb combines with hydrogens.
I have looked and found no literature discussing this and the ACLS protocols dont mention any issues either.
I did read that biarbs efficacy is in question because it may not address the true cause of the acidosis but didnt did much into this.

Thank you very much in advance!

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http://circ.ahajournals.org/content/122/18_suppl_3/S729.full.pdf said:
End-tidal CO2 is the concentration of carbon dioxide in exhaled air at the end of expiration. It is typically expressed as a partial pressure in mm Hg (PETCO2 ). Because CO2 is a trace gas in atmospheric air, CO2 detected by capnography in exhaled air is produced in the body and delivered to the lungs by circulating blood. Under normal conditions PETCO2 is in the range of 35 to 40 mm Hg. During untreated cardiac arrest CO2 continues to be produced in the body, but there is no CO2 delivery to the lungs. Under these conditions PETCO2 will approach zero with continued ventilation.

With initiation of CPR, cardiac output is the major determinant of CO2 delivery to the lungs. If ventilation is relatively constant, PETCO2 correlates well with cardiac output during CPR. The correlation between PETCO2 and cardiac output during CPR can be transiently altered by giving IV sodium bicarbonate.208 This is explained by the fact that the bicarbonate is converted to water and CO2 , causing a transient increase in delivery of CO2 to the lungs. Therefore, a transient rise in PETCO2 after sodium bicarbonate therapy is expected and should not be misinterpreted as an improvement in quality of CPR or a sign of ROSC.

Animal and human studies have also shown that PETCO2 correlates with CPP and cerebral perfusion pressure during CPR.209,210 The correlation of PETCO2 with CPP during CPR can be altered by vasopressor therapy, especially at high doses (ie, .1 mg of epinephrine).211–214 Vasopressors cause increased afterload, which will increase blood pressure and myocardial blood flow during CPR but will also decrease cardiac output. Therefore, a small decrease in PETCO2 after vasopressor therapy may occur but should not be misinterpreted as a decrease in CPR quality.

Persistently low PETCO2 values (,10 mm Hg) during CPR in intubated patients suggest that ROSC is unlikely.171,173,174,190,191,215,216 Similar data using quantitative monitoring of PETCO2 are not available for patients with a supraglottic airway or those receiving bag-mask ventilation during CPR. One study using colorimetic end-tidal CO2 detection in nonintubated patients during CPR found that low end-tidal CO2 was not a reliable predictor of failure to achieve ROSC.217 An air leak during bag-mask ventilation or ventilation with a supraglottic airway could result in lower measured PETCO2 values. Although a PETCO2 value of ,10 mm Hg in intubated patients indicates that cardiac output is inadequate to achieve ROSC, a specific target PETCO2 value that optimizes the chance of ROSC has not been established. Monitoring PETCO2 trends during CPR has the potential to guide individual optimization of compression depth and rate and to detect fatigue in the provider performing compressions.201,218,219 In addition, an abrupt sustained increase in PETCO2 during CPR is an indicator of ROSC.91,177,196,198–201 Therefore, it is reasonable to consider using quantitative waveform capnography in intubated patients to monitor CPR quality, optimize chest compressions, and detect ROSC during chest compressions or when rhythm check reveals an organized rhythm (Class IIb, LOE C). 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).
 
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Thank you for the link. Are you currently a resident? If so, have you observed this "transient" increase in ETCO2 and if so what kind of increase was observed? Was it such that ETCO2 became useless as a measure of good CPR and ROSC?

Thank you!
 
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No, I'm a 4th year. I've only been a part of pediatric codes, 2 of which bicarb was administered, but I don't recall monitoring changes in etco2 - not PALS certified so not sure if that's a part of PALS or not. The CC guys have mentioned on more than one occasion the concern for resp acidosis with bicarb, but not specifically with respect to ACLS
 
Etco2 goes up when you are getting the blood to peruse back to the lungs. Doesn't matter if you give bicarbonate or not. Won't go up unless you're circulating blood through the lungs. I never noticed it go up in the few times we monitor it. (I work in community, not academia). Honestly though I wouldn't worry too much. Only thing that ultimately works in the vast vast majority of cases is high quality cpr, appropriate defibrillation, airway, and starting it as quickly as possible. Epi, bicarbonate and most of the drugs in acts may improve rosc but may not improve survival to intact neurological outcome.
 
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ETCO2 would not go up as this measurement reflects exhaled CO2, if there is no or minimal flow (i.e. Cardiac arrest) then the ETCO2 will remain low. This is why ETCO2 is an early indicator of ROSC, flow improves suddenly and gas is available for exhalation=> spike in ETCO2. In reality there are very few reasons why Bicarb should be used, especially in cardiac arrest. Unless you can assure good gas exchange (highly unlikely in cardiac arrest), all the Bicarb is doing is increasing the amount of carbonic acid in solution (i.e. the blood). H20 + CO2 =H2CO3= CO2 + H2O. Also, the pKa of carbonic acid is ~6.2 so at best, its buffering ability is at the very edge of the most severely acidotic patients. You may want to look into THAM and CarbiCarb as alternative buffers which are actually CO2 consuming rather than CO2 producing buffers.
 
Awesome responses. Thank you very much. I was in a code the other night asking for ETCO2 to assess compressions and an ARNP shut me down stating the patient had received bicarb. I explained that I had never read literature that stated bicarb confounded the ETCO2 monitoring ect and looked for literature the next day. I figured I would ask those who would know the most, docs in the field.
Thank you. I'll have a better response in the future and stick to my guns when I know its in the best interest of our patient.
 
EM PGY-3 near the end of residency and an ACLS instructor.

Yes, bicarb technically can do the above -- but if you're giving bicarb, it's generally because there's either a specific need for it, or you're starting to take the kitchen sink approach.

I don't recall noticing any specific rise in EtCO2 with bicarb other than a little fluctuation -- and the ARNP who shut you down, IF he/she shut you down solely for that reason, was mistaken. Having given bicarb is a silly justification for not using quantitative EtCO2.
 
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EM PGY-3 near the end of residency and an ACLS instructor.

Yes, bicarb technically can do the above -- but if you're giving bicarb, it's generally because there's either a specific need for it, or you're starting to take the kitchen sink approach.

I don't recall noticing any specific rise in EtCO2 with bicarb other than a little fluctuation -- and the ARNP who shut you down, IF he/she shut you down solely for that reason, was mistaken. Having given bicarb is a silly justification for not using quantitative EtCO2.

Thank you very much! I spoke with my preceptor the next night and his response was similar to yours and rwmedics. I was told that the person who shut me down oversteps their boundaries and is overconfident in their knowledge of medicine in general. Its just another opportunity for me to learn not only medicine but how this whole team thing works in the moment. Its not perfect, lots of personalities ect. However, when Im in a situation like residency I will be more assertive when I know what Im trying to do is in the best interst of our patient and supported by evidence based medicine.
 
Agree with above- anesthesiology resident here; have been in OR cases with intermittent loss/return of circ and it was always very evident when we lost/got back circulation based on continuous etCO2-- despite having given bicarb. The bicarb's effect (maybe 5-10 mmhg if that) was way way smaller than the effect of ROSC (etCo2 in the teens --> 40s with ROSC).
 
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Awesome responses. Thank you very much. I was in a code the other night asking for ETCO2 to assess compressions and an ARNP shut me down stating the patient had received bicarb. I explained that I had never read literature that stated bicarb confounded the ETCO2 monitoring ect and looked for literature the next day. I figured I would ask those who would know the most, docs in the field.
Thank you. I'll have a better response in the future and stick to my guns when I know its in the best interest of our patient.
How do you as a physician get "shut down" by an NP?

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