Modeling the impact of ventilations on the capnogram in out-of-hospital cardiac arrest

Aim Current resuscitation guidelines recommend waveform capnography as an indirect indicator of perfusion during cardiopulmonary resuscitation (CPR). Chest compressions (CCs) and ventilations during CPR have opposing effects on the exhaled carbon dioxide (CO2) concentration, which need to be better characterized. The purpose of this study was to model the impact of ventilations in the exhaled CO2 measured from capnograms collected during out-of-hospital cardiac arrest (OHCA) resuscitation. Methods We retrospectively analyzed OHCA monitor-defibrillator files with concurrent capnogram, compression depth, transthoracic impedance and ECG signals. Segments with CC pauses, two or more ventilations, and with no pulse-generating rhythm were selected. Thus, only ventilations should have caused the decrease in CO2 concentration. The variation in the exhaled CO2 concentration with each ventilation was modeled with an exponential decay function using non-linear-least-squares curve fitting. Results Out of the original 1002 OHCA dataset (one per patient), 377 episodes had the required signals, and 196 segments from 96 patients met the inclusion criteria. Airway type was endotracheal tube in 64.8% of the segments, supraglottic King LT-D (TM) in 30.1%, and unknown in 5.1%. Median (IQR) decay factor of the exhaled CO2 concentration was 10.0% (7.8 - 12.9) with R-2 = 0.98(0.95 - 0.99). Differences in decay factor with airway type were not statistically significant (p = 0.17). From these results, we propose a model for estimating the contribution of CCs to the end-tidal CO2 level between consecutive ventilations and for estimating the end-tidal CO2 variation as a function of ventilation rate. Conclusion We have modeled the decrease in exhaled CO2 concentration with ventilations during chest compression pauses in CPR. This finding allowed us to hypothesize a mathematical model for explaining the effect of chest compressions on ETCO2 compensating for the influence of ventilation rate during CPR. However, further work is required to confirm the validity of this model during ongoing chest compressions.The Basque Government provided support in the form of a grant for research groups (IT1087-16) for authors Jose Julio Gutierrez, Jesus Maria Ruiz, Sofia Ruiz de Gauna, and Mikel Leturiondo; and in the form of a predoctoral grant (PRE-2017-2-0201) for author Mikel Leturiondo (https://www.euskadi.eus).The Spanish Ministry of Economy, Industry and Competitiveness provided support in the form of a grant for research projects (RTI2018-094396-B-I00) for authors Jose Julio Gutierrez, Jesus Maria Ruiz, Sofia Ruiz de Gauna, and Mikel Leturiondo; and in the form of the program Torres Quevedo (PTQ-16-08201) for author Digna Maria Gonzalez-Otero (http://www.ciencia.gob.es/).Bexen Cardio, a Spanish medical device manufacturer, provided support in the form of a salary for author Digna Mari ' a Gonza ' lez-Otero. None of the above funders had any additional role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific role of each author is articulated in the "author contributions" section. Authors James Knox Russell, Carlos Corcuera, Juan Francisco Urtusagasti, and Mohamud Ramzan Daya received no funding for this work

The Role of Chest Compressions on Ventilation during Advanced Cardiopulmonary Resuscitation

There is growing interest in the quality of manual ventilation during cardiopulmonary resuscitation (CPR), but accurate assessment of ventilation parameters remains a challenge. Waveform capnography is currently the reference for monitoring ventilation rate in intubated patients, but fails to provide information on tidal volumes and inspiration–expiration timing. Moreover, the capnogram is often distorted when chest compressions (CCs) are performed during ventilation compromising its reliability during CPR. Our main purpose was to characterize manual ventilation during CPR and to assess how CCs may impact on ventilation quality. Methods: Retrospective analysis were performed of CPR recordings fromtwo databases of adult patients in cardiac arrest including capnogram, compression depth, and airway flow, pressure and volume signals. Using automated signal processing techniques followed by manual revision, individual ventilations were identified and ventilation parameters were measured. Oscillations on the capnogram plateau during CCs were characterized, and its correlation with compression depth and airway volume was assessed. Finally, we identified events of reversed airflow caused by CCs and their effect on volume and capnogram waveform. Results: Ventilation rates were higher than the recommended 10 breaths/min in 66.7% of the cases. Variability in ventilation rates correlated with the variability in tidal volumes and other ventilatory parameters. Oscillations caused by CCs on capnograms were of high amplitude (median above 74%) and were associated with low pseudo-volumes (median 26 mL). Correlation between the amplitude of those oscillations with either the CCs depth or the generated passive volumes was low, with correlation coefficients of −0.24 and 0.40, respectively. During inspiration and expiration, reversed airflow events caused opposed movement of gases in 80% of ventilations. Conclusions: Our study confirmed lack of adherence between measured ventilation rates and the guideline recommendations, and a substantial dispersion in manual ventilation parameters during CPR. Oscillations on the capnogram plateau caused by CCs did not correlate with compression depth or associated small tidal volumes. CCs caused reversed flow during inspiration, expiration and in the interval between ventilations, sufficient to generate volume changes and causing oscillations on capnogram. Further research is warranted to assess the impact of these findings on ventilation quality during CPR.This research was funded by the grant PID2021-126021OB-I00 by MCIN/AEI/10.13039/501100011033 and by ERDF A way of making Europe, and by the grant IT1590-22 by the Basque Government. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Assessment of the evolution of end-tidal carbon dioxide within chest compression pauses to detect restoration of spontaneous circulation.

BackgroundMeasurement of end-tidal CO2 (ETCO2) can help to monitor circulation during cardiopulmonary resuscitation (CPR). However, early detection of restoration of spontaneous circulation (ROSC) during CPR using waveform capnography remains a challenge. The aim of the study was to investigate if the assessment of ETCO2 variation during chest compression pauses could allow for ROSC detection. We hypothesized that a decay in ETCO2 during a compression pause indicates no ROSC while a constant or increasing ETCO2 indicates ROSC.MethodsWe conducted a retrospective analysis of adult out-of-hospital cardiac arrest (OHCA) episodes treated by the advanced life support (ALS). Continuous chest compressions and ventilations were provided manually. Segments of capnography signal during pauses in chest compressions were selected, including at least three ventilations and with durations less than 20 s. Segments were classified as ROSC or non-ROSC according to case chart annotation and examination of the ECG and transthoracic impedance signals. The percentage variation of ETCO2 between consecutive ventilations was computed and its average value, ΔETavg, was used as a single feature to discriminate between ROSC and non-ROSC segments.ResultsA total of 384 segments (130 ROSC, 254 non-ROSC) from 205 OHCA patients (30.7% female, median age 66) were analyzed. Median (IQR) duration was 16.3 (12.9,18.1) s. ΔETavg was 0.0 (-0.7, 0.9)% for ROSC segments and -11.0 (-14.1, -8.0)% for non-ROSC segments (p ConclusionAverage percent variation of ETCO2 during pauses in chest compressions allowed for ROSC discrimination. This metric could help confirm ROSC during compression pauses in ALS settings