AAEM/RSA RESIDENT JOURNAL REVIEW
End-Tidal Carbon Dioxide Monitoring in Cardiopulmonary Resuscitation Christianna Sim, MD MPH; Taylor Conrad, MD MS; Taylor M. Douglas, MD; Wesley Chan, MD Editors: Kelly Maurelus, MD FAAEM and Kami Hu, MD FAAEM
Question: How can end-tidal carbon dioxide (ETCO2) monitoring guide our management of cardiac arrest? In 2010, the American Heart Association (AHA) revised the Advanced Cardiac Life Support (ACLS) guidelines to include the recommendation of using capnography to monitor end-tidal carbon dioxide (ETCO2) during cardiopulmonary resuscitation (CPR),1 and has continued this recommendation to date. Measured ETCO2 during cardiac arrest is a measure of the cardiac output generated by chest compressions but is affected by various other factors including endotracheal tube complications, ventilation, and medications administered. These issues notwithstanding, studies supporting ETCO2 as a surrogate marker of cardiac output outside of cardiac arrest2,3 indicate that ETCO2 could be a non-invasive, more readily available means of providing feedback in real time during resuscitation efforts. Previous studies have shown that low (<10 mmHg) ETCO2 values during resuscitation are predictive of mortality4,5,6 and that initial, average, and final ETCO2 are higher in successfully resuscitated patients,7,8 and there is an emerging possibility that ETCO2 could possibly even predict survival to discharge.7,9 Here we review some of the more recent literature regarding the use of ETCO2 during CPR and evidence on how it can guide resuscitation efforts.
Sheak KR, Wiebe DJ, Leary M, et al. Quantitative relationship between end-tidal carbon dioxide and CPR quality during both in-hospital and out-of-hospital cardiac arrest. Resuscitation. 2015;89:149-154. Based on previous studies that suggested ETCO2 as an indicator of cardiac output,2,3 Sheak et al. hypothesized that it may also reflect the quality of chest compressions (CC) during CPR, thus giving feedback on resuscitation efforts in real time. They specifically sought to investigate the relationship between ETCO2 and CC depth, CC rate, and ventilation rate in both in-hospital cardiac arrests (IHCA) and out-of-hospital cardiac arrests (OHCA). They conducted a prospective, multicenter study at hospital sites in the United States in which they were able to capture CPR-recording defibrillator and continuous side-stream CO2 data in patients with an advanced airway (endotracheal tube or laryngeal mask airway), regardless of the etiology of the cardiac arrest or initial rhythm, with at least two minutes of synchronized chest compressions and ETCO2 data. The data metrics were averaged over 15-second epochs. In total, their study included 583 cases, 227 (39%) IHCA and 356 (61%) OHCA. While chest compression rate did not significantly affect ETCO2, the depth of compressions was a significant predictor of ETCO2values independent of CC or ventilation rate. For every 10 mm increase in
42
COMMON SENSE NOVEMBER/DECEMBER 2020
depth there was an associated increase in ETCO2 by an average of 1.4 mmHg (p <0.001), independent of CC rate (slow, medium, fast). Perhaps unsurprisingly, ventilation rate was inversely related to ETCO2 values. Every additional 10 breath per minute increase in rate lowered ETCO2 by an average of 3.0 mmHg (p <0.001). The overall case-averaged mean ETCO2 values in those with ROSC were higher compared to those who did not achieve ROSC (34.5 ± 4.5 vs 23.1 ± 12.9 mmHg, p <0.001). They also observed a similar relationship seen in regard to survival to hospital discharge (38.2 ±12.9 vs 26.1 ±15.2 mmHg, p <0.001). The authors found a significant relationship between CC depth and ETCO2 and performed a fairly robust assessment, albeit not without limitations. The inability to assess for the effect ventilatory volume, without which minute ventilation cannot be calculated, leaves a possible confounder of the relationship between CC depth with ETCO2. They list other confounders they were unable to measure, such as the administration of epinephrine, the cause of cardiac arrest, underlying metabolic rate, and any metabolic derangements during the arrest. Also, because they did not know the relationship between the onset of resuscitation and initiation of active recording, they were unable to see if the CC depth- ETCO2 relationship differed depending on the phase of cardiac arrest care. To further understand the influence of CPR performance on ETCO2, there must be further investigations on how this relationship may be affected by these other factors. The authors highlighted the wide variability of the relationship between CC depth and ETCO2 posing a challenge to its applicability to all resuscitation events. As such, despite seeing a clear relationship between CPR quality (as indicated by depth of compressions) and ETCO2, there is no clear benchmark that can be set based on this data alone and would require further evidence to set a specific ETCO2 to aim for during resuscitation efforts.
Pokorná M, Necas E, Kratochvíl J, et al. A sudden increase in partial pressure end-tidal carbon dioxide (P(ET)CO(2)) at the moment of return of spontaneous circulation. J Emerg Med. 2010;38(5):614-621. While an increase in partial pressure ETCO2 has been observed after ROSC in both experimental and clinical studies, Pokarnoa et al. set out to determine whether an increase in ETCO2 could be used as a reliable indicator of ROSC in their retrospective case-control study. They looked at two extremes of patients experiencing OHCA: those who had single uncomplicated ROSC followed by stable spontaneous circulation and those with no signs of ROSC who died at the scene.
>>
