Understanding Pressure Excursions in Extracorporeal Technologies: The Role of Shear Stress and Hematologic Predisposition

Background: Mechanical forces within extracorporeal circulation systems such as cardiopulmonary bypass (CPB) and extracorporeal membrane oxygenation (ECMO) can profoundly alter blood physiology. Elevated pressure drops across membrane oxygenators generate abnormal shear stress capable of activating platelets through calcium-dependent mechanotransduction pathways. Activated platelets may adhere to oxygenator fibers, forming microaggregates that progressively increase resistance, impair gas exchange, and contribute to high pressure excursions (HPE). Understanding this mechanobiological loop is essential to improving oxygenator performance and patient safety. Materials and Methods: This narrative mini-review was developed through a structured literature search conducted in PubMed, Scopus, and Web of Science. Studies published in English and focusing on shear stress, platelet activation, and oxygenator function during extracorporeal life support were considered. Keywords included: “platelet activation,” “shear stress,” “extracorporeal circulation,” “ECMO,” “cardiopulmonary bypass,” “oxygenator failure,” “pressure drop,” “high pressure excursion,” “mechanotransduction,” and “platelet aggregation.” After title/abstract screening and full-text assessment, 13 articles met the inclusion criteria and were analyzed to synthesize current mechanistic and clinical evidence. Results: The literature shows that elevated shear stress within oxygenators can directly activate platelets independently of biochemical agonists. Shear-mediated calcium influx initiates platelet shape change, adhesion, and aggregation along hollow fibers, promoting progressive flow obstruction and increasing transmembrane pressure drop. This contributes to a self-reinforcing cycle in which rising resistance further elevates shear, amplifying platelet activation and accelerating oxygenator dysfunction. Conclusions: Shear-induced platelet activation represents a central mechanism in the development of pressure excursions and early oxygenator failure during extracorporeal support. Recognition of this mechanobiological cycle has important implications for oxygenator design, surface biocompatibility, anticoagulation management, and real-time monitoring strategies. A deeper understanding of platelet mechanotransduction may contribute to improving device longevity and enhancing clinical safety in CPB and ECMO.