Survival and neurological outcomes after out-of-hospital cardiac arrest (OHCA) remain low. The further development of prehospital extracorporeal resuscitation (ECPR) towards Controlled Automated Reperfusion of the Whole Body (CARL) has the potential to improve survival and outcome in these patients. In CARL therapy, pulsatile, high blood-flow reperfusion is performed combined with several modified reperfusion parameters and adjusted defibrillation strategies. We aimed to investigate whether pulsatile, high-flow reperfusion is feasible in refractory OHCA and whether the CARL approach improves heart-rhythm control during ECPR. In a reality-based porcine model of refractory OHCA, 20 pigs underwent prehospital CARL or conventional ECPR. Significantly higher pulsatile blood-flow proved to be feasible, and critical hypotension was consistently prevented via CARL. In the CARL group, spontaneous rhythm conversions were observed using a modified priming solution. Applying potassium-induced secondary cardioplegia proved to be a safe and effective method for sustained rhythm conversion. Moreover, significantly fewer defibrillation attempts were needed, and cardiac arrhythmias were reduced during reperfusion via CARL. Prehospital CARL therapy thus not only proved to be feasible after prolonged OHCA, but it turned out to be superior to conventional ECPR regarding rhythm control.

Controlled reperfusion by monitoring the blood pressure, blood flow, and specific blood parameters during extracorporeal reperfusion after cardiac arrest has the potential to limit ischemia–reperfusion injury. The intracellular calcium overload as part of the ischemia–reperfusion injury provides the possibility for the injury to be counteracted by the early suppression of serum calcium with the aim of improving survival and the neurological outcome. We investigated the effects of prolonged serum calcium suppression via sodium citrate during extracorporeal resuscitation using the CARL protocol (CARL—controlled automated reperfusion of the whole body) compared to a single-dose approach in a porcine model after prolonged cardiac arrest. A control group (N = 10) was resuscitated after a 20 min cardiac arrest, initially lowering the intravascular calcium with the help of a single dose of sodium citrate as part of the priming solution. Animals in the intervention group (N = 13) received additional sodium citrate for the first 15 min of reperfusion. In the control group, 9/10 (90.0%) animals survived until day 7 and 7/13 (53.8%) survived in the intervention group (p = 0.09). A favorable neurological outcome on day 7 after the cardiac arrest was observed in all the surviving animals using a species-specific neurological deficit score. The coronary perfusion pressure was significantly lower with a tendency towards more cardiac arrhythmias in the intervention group. In conclusion, a prolonged reduction in serum calcium levels over the first 15 min of reperfusion after prolonged cardiac arrest tended to be unfavorable regarding survival and hemodynamic variables compared to a single-dose approach in this animal model.

Small animal models are indispensable in cardiopulmonary resuscitation (CPR) research. High-quality CPR, characterized by consistent chest compression rate, depth, and positioning is crucial for survival. However, achieving standardization in manual high-frequency chest compressions in small animal models remains technically challenging. This study evaluated the reproducibility of manual chest compressions and introduced a novel mechanical chest compression device (MCD) designed to improve consistency in rodent experiments. In an in vitro setup, manual compressions were performed by ten participants at target rates ranging from 100 to 260 bpm, guided by a metronome. Compressions performed on a fluid-filled polymer reservoir were analyzed for the compression rate, variability, and time within a ± 10% target range. A color indicator was used to assess the variability of the compression point. A small animal MCD was designed and tested under the same conditions. In vivo, 5 Sprague-Dawley rats underwent 5 min of electrically induced normothermic cardiac arrest followed by 8 min of external chest compressions using the MCD. Obtained data was compared to the in vitro results. A total of 21,650 manual and 20,098 mechanical compressions were analyzed. At 200 bpm, chest compressions using the MCD were significantly more precise (201 ± 1.2 bpm) than manual compressions (218 ± 21 bpm, p < 0.001) with a significant reduced compression point variability (1.7 ± 0.1 cm ² vs. 10.8 ± 3.1 cm ² , p < 0.001). Manual compressions maintained target rate in 58.8% of time compared to 100% for the MCD. In vivo testing confirmed these findings with chest compressions remaining within the target range 100% of the time and showing minimal rate variability (1.8 ± 1.7 bpm). These results highlight the limitations of manual chest compressions and demonstrate the potential of the MCD to enhance standardization and reproducibility in rodent CPR research.