Extracorporeal cardiopulmonary resuscitation (ECPR) has emerged as a promising intervention for refractory cardiac arrest, with potential benefits in survival and neurological outcomes. However, the impact of ECPR’s rapid, non-pulsatile restoration of cerebral blood flow on intracranial physiology and autoregulation remains poorly understood.

Using a porcine model, this study investigated the dynamics of intracranial pressure (ICP), cerebral autoregulation, and pulsatility during key experimental phases: Baseline, Fibrillation, ECMO, and ROSC. ICP waveform features, including spectral entropy and centroid, were analyzed to assess signal complexity and dominant frequency shifts. Pressure reactivity index (PRx), the correlation between MAP and ICP, was used to assess impaired cerebral autoregulation (PRx > 0.3). Pulsatility, quantified by pulse pressure (PP) and pulsatility index (PI), was evaluated for its interaction with PRx.

Significant alterations in ICP and PRx were observed across experimental phases. During Fibrillation, ICP increased, waveforms lost pulsatile structure and complexity, and elevated PRx indicated impaired autoregulation. ECMO initiation resulted in a reduction of ICP fluctuations but reduced pulsatility due to the steady, non-physiological flow. Following ROSC, ICP pulsatility partially recovered, but PRx variability remained high, suggesting inter-subject differences in autoregulatory recovery. Negative correlations between pulsatility and PRx (slope = –0.096, 95% CI: –0.136 to –0.056, p = 3.07 × 10⁻⁶) suggested that pulsatility plays a critical role in autoregulatory function.

This study highlights the complex intracranial changes during ECPR, emphasizing the importance of pulsatility in maintaining cerebral autoregulation. Findings suggest the need for refined ECPR protocols to optimize cerebral protection and improve autoregulatory recovery.