End Tidal CO2 in Cardiac Arrest

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Written by: Alex Herndon, MD (NUEM PGY-2) Edited by: Andrew Moore, MD (NUEM Alum '18) Expert commentary by: Seth Trueger, MD, MPH

Introduction:

ER, Grey’s Anatomy, House, Chicago Med, The Good Doctor - across the nation millions tune in to their favorite medical dramas hoping to get a glimpse at what it’s like to be in the business of saving lives. As a newly minted emergency medicine intern, my eye caught on to the most recent addition, The Resident, intrigued by how the show would portray the medical profession. While watching and cringing at dramatized incidences of medical nonsense, one scene particularly stood out.

It was day one of residency and the new intern was leading the resuscitation of a patient who suddenly arrested. Fast-forward, the intern achieves return of spontaneous circulation, however he is immediately chastised by his senior resident who states, “her end-tidal CO2 was less than 15 for the entire code…”

As the credits rolled I was left agreeing with critic Dr. Esther Choo in that “this show feels like a most unfortunate and untimely addition to the medical drama genre”, given it is the least accurate medical show I’ve watched to date, except for this fleeting reference to End Tidal CO2 (ETCO2).

 

A Review of ETCO2 and its Applications:

Traditionally, ETCO2 has been used in order to assess proper endotracheal tube placement. Approximately 25 years ago anesthesiologists began using ETCO2 capnography because it was revealed that approximately 93% of anesthesia errors could have been prevented with additional capnography monitoring. In particular, the sensitivity of color change of colorimetric devices can be faulty at low concentrations of CO2, a particular concern when there is presumed decreased CO2 released from the lungs due to decreased cardiac output during an arrest, or if the ET tube is placed within the esophagus. The addition of capnography not only reinforces that the ET tube is properly placed, but its use has been extrapolated to indirectly assess cardiac output. (1)

 

The additional data ETCO2 supplies can be used in two key ways:

 

1. To assess quality of chest compressions

In cardiac arrest, ETCO2 waveform, while performing CPR, can serve as an indirect measurement of blood flow generated by chest compressions. The height of the ETCO2 waveform during CPR has been used as an indirect measure of adequate chest compressions, helping those involved in resuscitation monitor the effectiveness of their compressions in real time. In the awake adult, normal cardiac index lies between 2.5-4 L/min/m2, with an ETCO2 of 35-45 mmHg. On average during CPR, if adequate chest compressions are being delivered a cardiac index of 1.6-1.9 L/min/m2 can be generated, which correlates with ETCO2 pressures of 20mmHg.(1) ACLS guidelines define high quality chest compressions as achieving ETCO2 pressures of at least 10-20 mmHg. As rotating medical professionals deliver chest compressions, ETCO2 can be used to determine if they need to be deeper, if there is performer fatigue, or if there are other factors that might be inhibiting the ability to maintain ideal cardiac output outside of ineffective chest compressions. All in all, it provides a more accurate assessment of chest compression adequacy than visual estimation of compression depth.

 

2. To help predict return of spontaneous circulation (ROSC)

Numerous studies have shown that abrupt increases in ETCO2 pressures exceeding 10 mmHg that remain higher than preceding values suggest an increase in cardiac output and is indicative of ROSC, hence the incorporation of such measures in ACLS guidelines.(1) Patients with values less than 10 mmHg are more likely to die during CPR, and those with values greater than 10 during CPR were more likely to get ROSC. (1) However when comparing a mere 10 mmHg ETCO2 pressure to the minimal normal ETCO2 pressure of 35 mmHg, it can be difficult to argue 10 mmHg is enough. Multiple studies have aimed to drive this number up, in particular showing ETCO2 pressures higher than 16mHg were significantly associated with survival from CPR in the emergency department. However, the use of an absolute ETCO2 value was limited by the cause of cardiac arrest. Average ETCO2 pressures that achieved ROSC widely varied depending on whether cardiac arrest was purely cardiac versus pulmonary in etiology. (1) A 2015 meta-analysis of ETCO2 values associated with ROSC showed, on average, patients with ROSC after CPR had an average ETCO2 level of 25 mmHg, significantly higher than the current recommended 10 mmHg threshold.(2) Other than the aforementioned minimal ETCO2 threshold, it is important to follow ETCO2 trends, looking for the sudden increase in ETCO2 and maintenance of elevated levels associated with ROSC.

 

Furthermore, other studies have attempted to show how ETCO2 can be a tool in deciding to terminate CPR when ROSC isn’t achieved. One study from 1997 reported that ETCO2 less than 10 mmHg at the 20 minute mark is predictive of non-survivability in outside-hospital cardiac arrest patients thus should lead to terminating resuscitation efforts.(3) Current studies of use of ETCO2 in outside hospital arrest trends have shown 3-5 minutes of ETCO2 <10 mmHg are associated with a bad prognosis and has been used to terminate in-field resuscitation efforts.(4)

 

Next Steps:

While more data is needed in order to potentially reset the ETCO2 threshold used to assess adequate CPR and ultimately long-term survival post-arrest, others are looking at alternate applications of ETCO2. In 2016 Wang et al studied whether or not ETCO2 values could be used as a predictor of survival when looking at in-hospital versus outside-hospital cardiac arrests. They found that an initial ETCO2 level was predictive of not only sustained ROSC, but also survival to discharge.(2) Others have looked at the use of ETCO2 to determine potential effectiveness of defibrillation. It was found that ETCO2 less than 7 mmHg never resulted in effective shocks, whereas shocks delivered with ETCO2 greater than 45 mmHg were always successful. Ultimately the authors attributed the success to performing high quality chest compressions prior to defibrillation.(5)

 

Limitations of ETCO2 Capnography and Conclusions:

Similar to how ETCO2 can vary given the cause of cardiac arrest, ETCO2 can be influenced by other factors, thus altering how physicians interpret capnography. In particular, no studies have assessed the effect or epinephrine or sodium bicarbonate on ETCO2. Further complicating matters, the majority of cardiac arrest patients end up intubated, thus ventilator settings or over bagging can influence expired CO2 levels creating yet another confounding factor. These subtleties regarding ETCO2 need further exploration.   

Next time you are waiting for that outside-hospital cardiac arrest to roll through the Emergency Department entrance, arm yourself with ETCO2 capnography not only to aid your resuscitative efforts, but also help with your decision-making along the way. Its usefulness extends beyond simply achieving ROSC and has the potential to prognosticate whether patients will not only survive but thrive.


Expert Commentary:

Thanks for this nice overview of the data behind quantitative waveform ETCO2 in arrest. While it’s not the only tool in our armamentarium, it certainly can be helpful in assessing whether compressions are being effectively done, which can help the compressor modify their technique or location, add an element of motivation for the compressor, and help identify when the compressor is tiring out so we can switch someone else in before the official 2 minutes is up. Similarly, if there’s a big jump upward in the ETCO2 (eg, from 12 to 35), it’s reasonable to deviate from the usual 2 minutes and jump to a pulse check.

Using low ETCO2s is helpful in identifying futile codes; the general rule is that if the ETCO2 is consistently <10 after 20 minutes of well-done ACLS, the patient is very unlikely to come back. I find it important to point out that this is not a sensitive test, however, and many arrested patients will continue to have ETCO2 over 10 during long codes. I try to not get too focused on the ETCO2 as the only marker of when to terminate resuscitative efforts. Rather, it can help make a hard decision easier in some cases, but like most things, it’s not a magic bullet.

One other caution: don’t be mislead by a flat ETCO2 waveform during an arrest. If you don’t see any waves, then the airway is not in and either replace it or confirm intubation by other means (eg VL or gentle bougie insertion to holdup).

Here is a short screencast I put together back in 2013 on the 3 major uses of ETCOS: ETT confirmation, arrest, and monitoring in procedural sedation:

https://player.vimeo.com/video/57510987

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Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine, Northwestern University


How To Cite This Post

[Peer-Reviewed, Web Publication]   Herndon A, Moore A (2018, October 1). End Tidal CO2 in Cardiac Arrest.  [NUEM Blog. Expert Commentary by Trueger NS]. Retrieved from http://www.nuemblog.com/blog/ETCO2


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Resources

  1. Kodali, B. Urman, R. Capnography during cardiopulmonary resuscitation: Current evidence and future directions. J Emerg Trauma Shock. 2014 Oct-Dec: 7(4): 332-340. Doi: 10.4103/0974-2700.142778

  2. Wang, AY. Initial end-tidal CO2 partial pressure predicts outcomes of in-hospital cardiac arrest. Am J Emerg Med. 2016 Dec;34(12):2367-2371. doi: 10.1016/j.ajem.2016.08.052.

  3. Morshedi, B. The role of ETCO2 in termination of resuscitation. J Emerg Med Services. 2017 Dec. <http://www.jems.com/articles/print/volume-42/issue-12/features/the-role-of-etco2-in-termination-of-resuscitation.html>

  4. Venkatesh, H. Keating, E. Can the value of end tidal CO2 prognosticate ROSC in patients coding into emergency department with an out-of-hospital cardiac arrest. Emerg Med J. 2017 Mar; 34(3): 187-189. doi: 10.1136/emermed-2017-206590.1

  5. Savastano, S et al. End-tidal carbon dioxide and defibrillation success in out-of-hospital cardiac arrest. Resuscitation. 2017 Dec;121:71-75. doi: 10.1016/j.resuscitation.2017.09.010.

 

Posted on October 1, 2018 and filed under Pulmonary.