Ventilation during continuous compressions or at 30:2 compression-to-ventilation ratio results in similar arterial oxygen and carbon dioxide levels in an experimental model of prolonged cardiac arrest

Background In refractory out-of-hospital cardiac arrest, transportation to hospital with continuous chest compressions (CCC) from a chest compression device and ventilation with 100% oxygen through an advanced airway is common practice. Despite this, many patients are hypoxic and hypercapnic on arrival, possibly related to suboptimal ventilation due to the counterpressure caused by the CCC. We hypothesized that a compression/ventilation ratio of 30:2 would provide better ventilation and gas exchange compared to asynchronous CCC during prolonged experimental cardiopulmonary resuscitation (CPR). Methods We randomized 30 anaesthetized domestic swine (weight approximately 50 kg) with electrically induced ventricular fibrillation to the CCC or 30:2 group and bag-valve ventilation with a fraction of inspired oxygen (FiO 2 ) of 100%. We started CPR after a 5-min no-flow period and continued until 40 min from the induction of ventricular fibrillation. Chest compressions were performed with a Stryker Medical LUCAS® 2 mechanical chest compression device. We collected arterial blood gas samples every 5 min during the CPR, measured ventilation distribution during the CPR using electrical impedance tomography (EIT) and analysed post-mortem computed tomography (CT) scans for differences in lung aeration status. Results The median (interquartile range [IQR]) partial pressure of oxygen (PaO 2 ) at 30 min was 110 (52–117) mmHg for the 30:2 group and 70 (40–171) mmHg for the CCC group. The median (IQR) partial pressure of carbon dioxide (PaCO 2 ) at 30 min was 70 (45–85) mmHg for the 30:2 group and 68 (42–84) mmHg for the CCC group. No statistically significant differences between the groups in PaO 2 ( p = 0.40), PaCO 2 ( p = 0.79), lactate ( p = 0.37), mean arterial pressure (MAP) ( p = 0.47) or EtCO 2 ( p = 0.19) analysed with a linear mixed model were found. We found a deteriorating trend in PaO 2 , EtCO 2 and MAP and rising PaCO 2 and lactate levels through the intervention. There were no differences between the groups in the distribution of ventilation in the EIT data or the post-mortem CT findings. Conclusions The 30:2 and CCC protocols resulted in similar gas exchange and lung pathology in an experimental prolonged mechanical CPR model.