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 (CO 2) concentration, which need to be better characterized. The purpose of this study was to model the impact of ventilations in the exhaled CO 2 measured from capnograms collected during outof-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 CO 2 concentration. The variation in the exhaled CO 2 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 CO 2 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 CO 2 level between consecutive ventilations and for estimating the end-tidal CO 2 variation as a function of ventilation rate.