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

Jose Julio Gutiérrez, Jesus María Ruiz, Sofía Ruiz de Gauna, Digna María González-Otero, Mikel Leturiondo, James Knox Russell, Carlos Corcuera, Juan Francisco Urtusagasti, Mohamud Ramzan Daya

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


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™ 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 R2 = 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.

Original languageEnglish (US)
Article numbere0228395
JournalPloS one
Issue number2
StatePublished - Feb 1 2020

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General

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