Contribution of chest compressions to end-tidal carbon dioxide levels generated during out-of-hospital cardiopulmonary resuscitation.

Abstract

Characterise how changes in chest compression depth and rate affect variations in end-tidal CO₂ (ETCO₂) during manual cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrest (OHCA). Retrospective analysis of adult OHCA monitor-defibrillator recordings having concurrent capnogram, compression depth, transthoracic impedance and ECG, and with atleast 1,000 compressions. Within each patient, during no spontaneous circulation, nearby segments with changes in chest compression depth and rate were identified. Average ETCO₂ within each segment was standardised to compensate for ventilation rate variability. Contributions of relative variations in depth and rate to relative variations in standardised ETCO₂ were characterised using linear and non-linear models. Normalisation between paired segments removed intra and inter-patient variation and made coefficients of the model independent of the scale of measurement and therefore directly comparable. A total of 394 pairs of segments from 221 patients were analysed (33% female, median (IQR) age 66 (55-74) years). Chest compression depth and rate were 50.4 (43.2-57.0)mm and 111.1 (106.5-116.1)compressions per minute. ETCO₂ before and after standardization was 32.1 (23.0-41.4)mmHg and 28.5 (19.4-38.7)mmHg. Linear model coefficient of determination was 0.89. Variation in compression depth mainly explained ETCO₂ variation (coefficient 0.95, 95% confidence interval (CI): 0.93-0.98) while changes in compression rate did not (coefficient 0.04, 95% CI: 0.01-0.07). Non-linear trend analysis confirmed the results. This study quantified the relative importance of chest compression characteristics in terms of their impact on CO₂ production during CPR. With ventilation rate standardised, variation in chest compression depth explained variations in ETCO₂ better than variation in chest compression rate.