Exploring weaning-related shock: Cardiac injury and overload, platelet-endothelial cell activation, and inflammatory response markers following ECMO decannulation

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Introduction Mortality in patients receiving Extracorporeal Membrane Oxygenation (ECMO) is partly attributable to unanticipated hemodynamic instability after elective decannulation, termed weaning-related shock (WRS). This study explored the etiology of WRS by analyzing sequential plasma biomarker profiles. Methods We analyzed a prospective cohort (2011–2022) of consecutive patients weaned from veno-arterial (V-A) or veno-venous (V-V) ECMO to evaluate WRS occurrence. WRS was defined as a rise in Vasoactive Inotropic Score ≥15 points for >6 h with a positive fluid balance and lactate >2 mmol/L within 72 h post-decannulation. Shock etiology was adjudicated as hemorrhagic, cardiogenic, septic, or unclassifiable. Subsequently, key plasma biomarkers reflecting inflammation, platelet-endothelial cell activation, and cardiac injury and overload were assessed pre- and post-decannulation, stratified on WRS occurrence, apparent etiology, and ECMO mode. Results Out of 97 eligible individuals, 88 (91%) were analyzed (70 V-A and 18 V-V). Among them, 24 (27%) patients developed WRS, all of whom had received V-A ECMO. WRS was attributed to hemorrhagic, cardiogenic, septic, or unclassifiable causes in 0, 8, 8 and 8 cases, respectively. No differences were observed between groups in markers of inflammation or platelet-endothelial cell activation, nor in their trajectories over time. Conversely, NT-proBNP levels, but not HsTnI, increased significantly after decannulation in WRS patients compared to V-V or V-A ECMO patients without WRS ( p = 0.003 and p = 0.02, respectively). NT-proBNP was also higher in these subjects prior to decannulation (all p < 0.001). Conclusion Biomarker responses following ECMO decannulation suggest cardiac overload as the primary driver of WRS, irrespective of clinical shock diagnosis.

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